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Head and neck radiology > Cerebrovascular diseae > Flashcards

Cerebrovascular diseae Flashcards

1
Q

Clinical term applies to any abrupt nontraumatic brain insult- literally a blow from an unseen hand

A

Stroke

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2
Q

2/3 of infarct are from

A

Thrombi

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3
Q

Normal brain metabolism is how many ml/100g tissue/min

A

55 ml/100g tissue/min

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4
Q

Oligemia is more common in the gray matter due to

A

Gray matter receives 3-4x more blood flow than white matter

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5
Q

Why are watershed zones more prone to infarction

A

They are served by penetrating end arteries and have no alternate route for perfusion

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6
Q

Mechanism of cytotoxic edema

A

Failure of membrane pumps permits efflux of K+ and simultaneous influx of Ca, Na and water, causing increased water content in the affected region

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7
Q

Cytotoxic edema peaks at how many days post infarction, and is maximum in what brain matter

A

3-7 days in gray matter

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8
Q

Vasogenic edema primarily affects what brain matter

A

White matter due to lose endothelial cell integrity

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9
Q

A subtle but important blurring of the gray white layers of the insula due to early edema. Can be seen in CT done within 6 hours of MCA occlusion

A

Insular ribbon sign

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10
Q

Hyperintense light bulb sign signal in DWI can be seen as early as how many minutes post infarction

A

15 minutes

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11
Q

T2 hyperintense signal from infarct will develop how many hours post ictus

A

6-12 hours post ictus

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12
Q

IV t-PA is frontline therapy for patients within how many hours of symptom onset

A

4.5 hours

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13
Q

endovascular thrombectomy can be done within how many hours of symptom onset

A

24 hours

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14
Q

ASPECTS score that can be a considered a candidate for thrombolysis

A

7 to 10

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15
Q

may be useful in identifying ischemic but still salvageable tissue (ischemic penumbra) to successfully guide selection of patients for stent retriever therapy beyong 4.5 hours

A

perfusion sensitive CT and MR techniques

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16
Q

this MRI sequence reflects “pure” diffusion behavior, free of underlying T2 contributions (“shine through” or “dark through”)

A

ADC

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17
Q

peak of edema in infarct as well encephalomalacic changes occur in what days

A

3-7 days

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18
Q

“fogging effect” may be encountered on CTs done during what week after infarction as edema and mass effect are subsiding

A

2nd week

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19
Q

edema that persists beyong __ month/s effectively rules out simple ischemia and should raise the possibility of recurrent infarction or an underlying tumor

A

1 month

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20
Q

pathophysiology of hemorrhagic transformation

A

reperfusion into infarcted capillary beds may secondarily lead to gross or microscopic hemorrhage, microscopic leakage of RBC (diapedesis), physical disruption of the capillary endothelial cells, loss of vascular autoregulation and anticoagulation or thrombolytic use

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21
Q

difference of hemorrhagic infarction from hemorrhagic transformation

A

hemorrhagic infarction is confined to the territory of the infarcted vessel, wheras primary hemorrhage does not necessarily respect vascular boundaries

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22
Q

true or false: IVH is uncommonly seen with hemorrhagic transformation and should raise the posibility of another process (such as hypertensive bleed or a ruptured AVM)

A

true

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23
Q

peak time of hemorrhagic transformation

A

1 to 2 weeks

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24
Q

appearance of hemorrhagic transformation

A

serpiginous line of petechial blood ff the gyral contours of the infarcted cortex. the dots are often patchy and discontinuous (petechial gyral pattern)

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25
Q

this event underlies both hemorrhagic transformation and contrast enhancement of infarctions

A

blood brain barrier breakdown

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26
Q

CT detected enhancement of infarcted brain parenchyma typically begins at about what week and peaks at how many days

A

1 week and peaks at 7 to 14 days

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27
Q

enhancement fades in infarct when gliosis ensues and BBB is repaired, and then resolves by what month

A

3 months

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28
Q

intravascular enhancement on MR is commonly seen in the infarcted territory during what week

A

1st week; seen in a majority of cortical infarcts at 1 to 3 days, and resolves by 10 days

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29
Q

virtually all cortical infarcts enhance by MR at __ weeks

A

2 weeks

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30
Q

Elster rule of 3s in cortical infarct enhancement in MR

A

parenchymal enhancement peaks at 3 days to 3 weeks and resolves by 3 months

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31
Q

patterns of ischemic events

A

diffuse (hypoxic-ischemic injury), multifocal (vasculitis, emboli), or focal (single embolism or thrombus)

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32
Q

Minutes post infarct CT and MR findings

A

CT- no changes

MR- absent flow void, arterial enhancement (1 to 10 days), DWI shows high signal

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33
Q

2-6 hours post infarct CT and MR findings

A

CT- hyperdense artery sign, insular ribbon sign

MR- brain swelling (T1), subtle T2 hyperintensity

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34
Q

6 to 12 hours post infarct CT and MR findings

A

CT- sulcal effacement, +/- decreased attenuation

MR- T2 hyperintensity

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35
Q

12 to 24 hours post infarct CT and MR findings

A

CT- decreased attenuation

MR- T1 hypointensity

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36
Q

3 to 7 days post infarct CT and MR findings

A

CT- maximum swelling

MR- maximum swelling

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37
Q

3 to 21 days post infarct CT and MR findings

A

CT- gyral enhancement (peak 7 to 14 days)

MR- gyral enhancement (peak 3 to 21 days) petechial methemoglobin

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38
Q

30 to 90 days post infarct CT and MR findings

A

CT and MR- encephalomalacia, loss of enhancement, resolution of petechial blood

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39
Q

classically, strokes and TIAs are divided into

A

anterior (carotid territory) or posterior (vertebrobasilar territory)

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40
Q

carotid endarterectomy can be done in anterior circulation infarcts if the carotid is narrowed by at least how many percent compared to its normal diameter

A

70%

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41
Q

ischemia in this territory may cause visual changes, aphasia, or sensorimotor deficits due to retinal, cortical or subcortical damage

A

carotid artery

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42
Q

strokes in this territory more likely to cause syncope, ataxia, cranial nerve findings, homonymous visual field deficits and facial symptoms opposite those of the body

A

vertebrobasilar strokes

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43
Q

occlusion of ophthalmic branch of ICA may cause

A

transient monocular blindess (amaurosis fugax)

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44
Q

atherosclerotic disease in this carotid segment is responsible for the majority of ischemic events in ICA territory

A

carotid bifurcation

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45
Q

carotid hemodynamic effects begin to be seen when there is ___% reduction in area or ___ % decrease in diameter

A

> 70% stenosis, <30% narrowing

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46
Q

gold standard for pre procedure carotid artery evaluation, but is being replaced by noninvasive studies in many centers

A

common carotid angiography

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47
Q

terminal bifurcation of ICA is into the

A

Anterior and middle cerebral arteries

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48
Q

serves the rostral portions of the basal ganglia

A

medial lenticulostriates

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49
Q

these branches supply the corpus callosum

A

pericallosal branches

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50
Q

branches that supply the medial aspects of the frontal and parietal lobes

A

hemispheric branches

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51
Q

5% of infarcts involve the

A

ACA

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52
Q

supplies the anterior-inferior aspect of the internal capsule, putamen, globus pallidus, caudate head, and portions of hypothalamus and optic chiasm

A

medial lenticulostriates

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53
Q

largest of the medial lenticulostriates that supply the caudate head/anterior internal capsule region

A

recurrent artery of Heubner

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54
Q

infarctions in the medial lenticulostriate territory may cause

A

problems with speech production (motor aphasia), facial weakness, and disturbances in mood and judgement

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55
Q

frontal pole branches of the ACA

A

orbitofrontal and frontopolar arteries

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56
Q

ACAs terminate as a bifurcation into the _____. these arteries run parallel to the corpus callosum from front to back, giving supply to the medial cortex of the frontal and parietal lobes

A

lower pericallosal and upper callosomarginal branches

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57
Q

branches that courses around and feeds the corpus callosum

A

pericallosal artery

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58
Q

unilateral damage in the ACA hemispheric branches will cause _____ on the opposite side of the body

A

preferential leg weakness

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59
Q

bilateral ACA infarction lead to

A

incontinence and an awake but apathetic state known as akinetic mutism

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60
Q

infarction in this area can cause a variety of interhemispheric disconnections syndromes

A

infarction of corpus callosum

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61
Q

artery that is host to almost 2/3 of infarcts

A

MCA

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62
Q

supplies most of the basal ganglia

A

lateral lenticulostriates

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63
Q

supplies the lateral cerebral surface

A

hemispheric branches

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64
Q

arise from the proximal MCA as numerous small perforating end-arteries distributed to the putamen, lateral globus pallidus, superior half of the internal capsule and adjacent corona radiata

A

lateral lenticulostriates

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65
Q

infarcts in these regions are commonly asymptomatic or may affect contralateral muscle tone and motor control

A

isolated vascular lesions of the globus pallidus or putamen

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66
Q

interruption of visual connections to the lateral geniculate nucleus results in

A

subtle type of contralateral homonymous hemianopsia

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67
Q

conduction aphasia or the inability to repeat, read aloud, despite preserved comprehension and fluency is due to infarction in the

A

arcuate fasciculus pathway from Wenicke to Broca speech areas

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68
Q

insula is supplied by

A

hemispheric branches

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69
Q

early presence of insular ribbon sign is due to

A

insular region is the farthest from any potential collateral supply when proximal MCA is occluded

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70
Q

supplies the anterolateral tip of the temporal lobe

A

anterior temporal artery

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71
Q

supplies the frontal lobe

A

operculofrontal arteries

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72
Q

supplies the motor and sensory strips

A

central sulcus arteries

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73
Q

supplies the parietal lobe behind the senosry strips

A

posterior parietal artery from posterior hemispheric branches of MCA

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74
Q

supplies the posterolateral parietal and lateral occipital lobes

A

angular artery

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75
Q

supplies majority of the temporal lobe

A

posterior temporal artery

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76
Q

occlusion of the rostral MCA branches of the dominant hemisphere will cause

A

motor/Broca aphasia

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77
Q

supplies the Wernick area

A

posterior branches of MCA in the dominant hemisphere

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78
Q

occlusion to this MCA branch may interrupt visual radiations, causing contralateral homonymous field defects

A

posterior temporal branch occlusion

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79
Q

infarction of these areas will produce contralateral weakness which affects face and arm more than leg

A

either hemispheres’s precentral gyrus

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80
Q

contralateral cortical sensory loss occurs when these areas are affected

A

the primary or association sensory cortex behind the central sulcus is affected

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81
Q

infarct in this area causes confusional states, bizarre impairment in visuospatial abilities and sometimes neglect (nonrecognition) of the left body

A

nondominant right hemisphere posterior MCA infarcts

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82
Q

complete occlusion of this artery cause these combination of deficits contralateral face and arm hemiparesis, field defect, either neglect or global aphasia, depending on which hemisphere is affected

A

MCA

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83
Q

If MCA stem is occluded because of internal capsule involvement, this symptom is apparent

A

leg weakness

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84
Q

VA originate from

A

subclavian arteries

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85
Q

VA ascend upward in the transverse foramina of what cervical level and turns sharply at what level

A

C6-C3, turns at C2-C1 foramen magnum levels

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86
Q

VA unites at what level to form Basilar artery

A

anterior to the low medulla

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87
Q

narrowing of cervical portions of the VA may be due to

A

compressive uncovertebral osteophytes

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88
Q

remains mainstay of tx for VB ischemia

A

anticoagulation and antiplatelet agents

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89
Q

leg weakness can be seen in what region of insult

A

either hemispheric ACA branch

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90
Q

incontinence, akinetic mutism may be seen in what arterial branch

A

both hemispheric ACA branches

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91
Q

facial weakness may be seen in what arterial branch

A

either medial lenticulostriates of ACA

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92
Q

dysarthria, with or without motor aphasia may be seen in what arterial branch

A

left medial lenticulostriates of ACA

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93
Q

face and arm > leg weakness may be seen in what arterial branch

A

either hemispheric branch of MCA

94
Q

motor aphasia, receptive aphasia, global aphasia may be seen in what arterial branch

A

left hemispheric branch of MCA

95
Q

neglect syndrome, visuospatial dysfunction may be seen in what arterial branch

A

right hemispheric MCA branch

96
Q

variable lacunar syndromes may be seen in what arterial branch

A

either lateral lenticulostriates of MCA

97
Q

hemianopsia may be seen in what arterial branch

A

eithr hemispheric PCA

98
Q

cortical blindness, memory deficits may be seen in what arterial branch

A

both hemispheric PCA

99
Q

somnolence and sensory disturbances may be seen in what arterial branch

A

either thalamoperforators of PCA

100
Q

ataxia, vertigo, vomiting, coma if mass effect with or without brainstem deficits may be seen in what arterial branch

A

either PICA, AICA or SCA of cerebellar arteries

101
Q

man in barrel syndrome may be seen in what arterial branch

A

wither ACA/MCA/PCA (watershed)

102
Q

severe memory problems may be seen in what arterial branch

A

bilateral ACA/MCA/PCA (watershed)

103
Q

sends large branches to the cerebellum and smaller perforating vessels to the brainstem

A

basilar artery

104
Q

occlusion of this artery is usually rapidly fatal, due to infarction of respiratory and cardiac centers in the medulla

A

basilar artery

105
Q

occlusion of perforating end arteries of BA causes focal brainstem infarction, usually manifest as ____. these lesions often extends to the ventral surface

A

cranial nerve dysfunction, ataxia, somnolence, and crossd motor or sensory deficits

106
Q

metabolic disturbances and hypertensive hemorrhages most commonly in the pns tend to be more located where

A

centrally and diffusely located

107
Q

locked in state is associated with large or multiple lesions in the

A

pons

108
Q

BA ends at its bifurcation into ___ at the midbrain level, just above the tentorial hiatus

A

PCA

109
Q

major branches of PCA

A

midbrain and thalamic perforating vessels, posterior choroidal arteries, cortical branches to the medial temporal and occipital lobes

110
Q

10 to 15% of infarcts occur at what vessel

A

PCA

111
Q

infarction in this part of brainstem leads to loss of pupillary light responses, impaired gaxe and somnolence

A

midbrain, due to the damage of the quadrigeminal plate, third cranial nerve nuclei, RAS formation

112
Q

most common problem in thalamic infarction

A

contralateral sensory loss

113
Q

supply the choroid plexus of third and lateral ventricles, pineal gland, regions contiguous with the third ventricle

A

posterior choroidal artery from proximal PCA

114
Q

supplies the inferomedial temporal lobe

A

inferior temporal arteries from PCA cortical branches

115
Q

superior occipital gyrus is supplied by

A

parieto-occipital artery from PCA cortical branches

116
Q

visual cortex of the occipital lobes is supplied by

A

calcarine artery from PCA cortical branches

117
Q

bilateral inferomedial infarction may cause

A

memory deficits

118
Q

loss of the primary visual cortex causes

A

complete loss of vision in the opposite visual field (homonymous hemianopsia)

119
Q

condition found in 20% if patients, in which one or both of the proximal P1 PCA segments may be hypoplastic or absent. in these cases, flow is derived from the ICA system via a prominent posterior communicating artery. this is commonly referred to as

A

fetal origin of PCA, since embryologiclly, the PCA develops with the ICA

120
Q

headache, vertigo, nausea, vomiting and ipsilateral ataxia are hallmarks of what region of infarct

A

cerebellar infarct

121
Q

management of cerebellar infarction or hemorrhage

A

posterior fossa decompression

122
Q

upper parts of cerebellum are supplied by

A

superior cerebellar arteries

123
Q

SCA territory includes

A

superior vermis, middle and superior cerebellar peduncles and superolateral aspects of the cerebellar hemisphere

124
Q

these arteries arise from proximal BA to supply the anteromedial cerebellum and sometimes part of the middle cerebellar peduncle

A

AICA

125
Q

usually the smallest of the 3 major cerebellar hemisphere branches

A

AICA

126
Q

occlusion of this cerebellar artery causes ipsilateral limb ataxia, nausea, vomiting, dizziness and headache

A

AICA

127
Q

bottom of the cerebellum is supplied by

A

PICA

128
Q

it is the first major intracranial branche of the VB system, usually arising from the distal vertebral artery, 1 to 2 cm below the basilar origin

A

PICA

129
Q

PICA territory includes

A

dorsolateral medulla, inferior vermis, and posterolateral cerebellar hemisphere

130
Q

AICA-PICA loop means

A

PICA maintains a reciprocal relation with AICA above it. if PICA is large, then the ipsilateral AICA is usually small, and vice versa

131
Q

usually the largest cerebellar hemispheric branch and is the most commonly infarcted cerebellar artery

A

PICA

132
Q

Wallenberg syndrome, including ataxia, facial numbness, Horner syndrome , dysphagia and dysarthria are seen in what region of brain and artery

A

medulla, PICA

133
Q

an episode of transient global hypoperfusion may result in infarctions at what regions

A

watershed regions between arterial territories

134
Q

typical triggering events in watershed infarcts

A

cardiac arrest, massive bleeding, anaphylaxis, surgery under general anesthesia

135
Q

these are regions perfused by terminal branches of 2 adjacent arterial territories

A

watershed zones

136
Q

imaging shows a string of small deep white matter lesions (“rosary bead sign”) or damage extending out from the “corners: of the lateral ventricles on higher sections in these infacted regions

A

watershed infarcts

137
Q

characteristic clinical findings include weakness isolated to the upper arms (man in a barrel syndrome) , cortical blindness and memory loss

A

watershed infarcts

138
Q

these are small subcortical infarcts that may occur in any territory. accounts for 15 to 20% of strokes

A

lacunes

139
Q

size of lacunes

A

2-5 mm3 cavities

140
Q

lacunar infarcts result from unfarction of

A

penetrating arteries

141
Q

pure motor or sensory syndromes may occur with these infarcts

A

lacunar infarct

142
Q

these infarcts are common in patients with history of long standing hypertension, leading to lipohyalinosis of the vessels and eventual thrombosis

A

lacunar infarcts

143
Q

characteristic locations of lacunar infarcts

A

lenticular nucleus 37%, pons 16%, thalamus 14%, caudate 10%, IC/corona radiata 10%

144
Q

isolated lesions in the anterior limb of IC interrupt connections to the

A

anterior frontal lobe

145
Q

begining at the genu of IC and posterior IC, it carries the

A

corticobulbar, head,arm, and then leg fibers in somatotopically organized fashion

146
Q

lesions in what part of IC are clinically most important since they may cause severe sensory, motor or mixed deficits

A

posterior limb of IC

147
Q

lesions at this part of the IC may disrupt speech production or swallowing, but generally become apparent only when bilateral

A

genu

148
Q

refers to state of multiple lacunar infarcts

A

etat lacunaire

149
Q

refers to enlarged perivascular spaces (Virchow-robin spaces) that may develop around perforating vessels

A

etat crible

150
Q

Virchow-robin spaces should follow these features

A

follow CSF intensity in all sequences, have no associated mass effects, occur along the path of a penetrating vessel

151
Q

common locations for Virchow-robin spaces

A

medial temporal lobes, inferior 1/3 of the putamen and thalamus, sometimes seen aong the course of small medullary veins near the vertex

152
Q

most perivascular spaces seen on MR are between how many mm

A

1 and 3 mm, some up to 5 mm or larger

153
Q

DWI in acute infacrt may remain hyperintense for about how many months

A

1 month

154
Q

these are commonly associated with patchy or diffuse T2 hyperintensities in the centrum semiovale

A

small vessel ischemic changes (UBOs)

155
Q

small vessel ischemic changes are also called

A

white matter hyperintensities, small vessel ischemic disease, senescent change, Binswanger disease, multi-infarct dementia and leukoariosis

156
Q

these conditions have been linked to reversible cerebral vasoconstrction syndrome, which can mimic vasculitis

A

Drug exposure (heroin, amphetamines, serotonin reuptake inhibitors), migraine and post ictal states

157
Q

this syndrome causes irregular beading of vessels but usually without the inflammatory infiltration of the vessel wall characteristic of vasculitis

A

reversible cerebral vasoconstrction syndrome

158
Q

vasculitis may be trigerred by

A

autoimmune disorders, polyarteritis nodosa, idiopathic processes

159
Q

management of vasculitis

A

steroids or cytotoxic drugs, RCVS is manged with vasodilators and removal of underlying trigger

160
Q

these infarcts occur in younger patients who present with headache, sudden focal deficits, and often seizures

A

venous infarcts

161
Q

predisposing factors in venous infarcts

A

hypercoagulable states, pregnancy, infection (spread from contiguous scalp, face, middle ear or sinus), dehydration, meningitis, and direct invasion by tumor

162
Q

common sinuses affected in venous infarcts

A

superior sagittal, transverse, straight sinus and cavernous sinus, either alone or in combination

163
Q

pattern of hemorrhagic infarction in venous versus arterial

A

venous- deep cortical or subcortical regions, they tend to be rounded and may spare some overlying cortex
arterial- classic wedge-shaped which grow larger toward the surface

164
Q

empty delta sign in venous clot is usually seen at what weeks

A

1 to 4 weeks after sinus occlusion

165
Q

empty delta sign may be confused if CT scanning is delayed for more than 30 min after contrast infusion due to

A

differential blood pool clearance and dural absorption of contrast, effectively highlighting the dural margins of a normal venous sinus

166
Q

best imaging evaluation for venous clots

A

spin-echo MR and MR venography

167
Q

MR sequence used for SAH

A

FLAIR

168
Q

MR sequence used in parenchymal hemorrhage

A

GRE

169
Q

better imaging modality for detection of subacute or chronic hemorrhage

A

MR

170
Q

MR signal generated by blood depends on a complex interplay of

A

hematocrit, oxygen content, type of hemogobin and chemical state of its iron-containing moieties, tissue pH, protein content of any clot formed, and integrity of RBC membranes

171
Q

oxygenated hemoglobin is sequentially converted to ____ over time

A

deoxyhemoglobin, methemoglobin and hemosiderin

172
Q

a small halo of surrounding edema is common in what phase of parenchymal bleeds

A

subacute

173
Q

iron within hemorrhage breakdown products changes the effective local magnetic field, a process known as

A

magnetic susceptibility

174
Q

key to the diagnosis of amyloid angiopathy is

A

identification of numerous additional punctate old hemorrhages on GRE, distributed peripherally, in the cortex, and near the gray-white junction

175
Q

hypertensive hemorrhage typically involves the

A

deep gray structures, especially thalami and BG

176
Q

oxyhemoglobin appears as high SI on T2 because

A

it is diamagnetic, containing ferrous ions

177
Q

deoxyhemoglobin causes accelerated dephasing of spins on T2 and GRE which results in signal loss because

A

it is paramagnetic, but it also containes ferrous ions

178
Q

oxyhemoglobin conversion to deoxyhemoglobin occurs over how many hours and is dependent on

A

local pH and oxygen tension

179
Q

in parenchymal or extraaxial hemaotma, further oxidation of deoxyhemoglobin leads to formation of

A

methemoglobin

180
Q

methemoglobin is what type of magnetism

A

ferric paramagnetic substance

181
Q

methemoglobin transformation occurs when

A

several days or longer, parallel in time course to lysis of RBCS

182
Q

this type of hemoglobin causes a makred acceleration of T1 relaxation, leading to bright signal on T1

A

methemoglobin

183
Q

this type of hemoglobin contained within intact RBC is able to set up local field gradients between the cell and the protons outside, leading to signal loss on T2

A

methemoglobin

184
Q

helpful indicator of subacute blood products

A

bright T1 signal

185
Q

methemoglobin is in early intracellular if it appears what on T2

A

low SI

186
Q

methemoglobin is extracellular if it appears what on T2

A

bright

187
Q

T2 of subacute hematomas show _____, in which a dependent later of intact cells exhibits dark signal and a plasma supernatant showing bright signal

A

hematocrit effect

188
Q

RBC and hemoglobin state in <1 day

A

intact RBC, oxyhemoglobin

189
Q

oxyhemoglobin appearance on T1 and T2

A

iso or dark T1, Bright T2

190
Q

RBC and hemoglobin state in 0-2 days

A

intact, deoxyhemoglobin

191
Q

deoxyhemoglobin appearance on T1 and T2

A

iso or dark T1, dark T2

192
Q

RBC and hemoglobin state in 2- 14 days

A

intact, methemoglobin (intracellular)

193
Q

intracellular methemoglobin appearance on T1 and T2

A

T1 bright, T2 dark

194
Q

RBC and hemoglobin state in 10-21 days

A

lysed, methemoglobin (extracellular)

195
Q

extracellular methemoglobin appearance on T1 and T2

A

T1 bright, T2 bright

196
Q

RBC and hemoglobin state in > 21 days

A

lysed, hemosiderin/ferritin

197
Q

appearance of hemosiderin in T1 and T2

A

T1 iso/dark, T2 dark

198
Q

hemosiderin is what type of magnetism

A

paramagentic ferric that is insoluble in water

199
Q

occasionally, large or recurrent SAHs will lead to diffuse hemosiderin deposition on the brain surface, a condition known as

A

superficial hemosiderosis or superficial siderosis

200
Q

CSF-lined compartment which surrounds the blood vessels and communicates with the ventricular system

A

Subarachnoid space

201
Q

unruptured pcom aneurysm may present as

A

unilateral 3rd nerve palsy

202
Q

unruptured ICA/parasellar aneurysm may present as

A

cavernous sinus syndrome

203
Q

unruptured acom aneurysm may present as

A

optic chiasmal syndrome (bitemporal field defect)

204
Q

berry aneurysms often occur where

A

near branch points of circle of Willis, 85% from anterior part of circle of Willis, while 15% arise in vertebrobasilar territory. branch points near acom (33%), MCA (30%), pcom (25%) and basilar (10%)

205
Q

when distal aneurysm is seen, what must be considered

A

prior history of trauma, systemic infection

206
Q

most sensitive places to look for SAh on CT

A

dependent portions of the subarachnoid spaces– interpeduncular fossa, posterior sylvian fissure, far posterior aspects of occipital horns

207
Q

if SAH cannot be detected due to patient;s low hematocrit, or the amount of hemorrhage is small or with delayed scanning, this procedure can confirm a suspected SAh

A

detection of RBCs or xanthocromia by lumbar puncture

208
Q

how to know the ruptured aneurysm if there are multiple aneurysms

A

one that is largest or more irregular, has focal mass effect, intra-aneurysmal clost, or shows change on serial examinations

209
Q

much feared complication in early clipping or coiling of aneurysm

A

vasospasm

210
Q

true or false: parenchymal bleeds generally have a higher initial mortality than infarcts, but on recovery show fewer deficits than a similar-sized infarct

A

true

211
Q

hypertensive hemorrhage are common in these areas

A

putamen (35 to 50%), subcortical white matter (30%), cerebellum (15%), thalamus (10 to 15%), pons (5 to 10%)

212
Q

primary predisposing factor to hypertensive hemorrhage

A

lipohyalinosis of vessels

213
Q

four main subtypes of vascular malformations

A

AVMs, cavernous malformations, telangiectasias and venous malformations

214
Q

these are high flow lesions and the most common type of brain vascular malformation

A

AVM

215
Q

common location of AVMs

A

supratentorial

216
Q

dilated capillary-sized vessels usually diagnosed at autopsy

A

telangiectasias

217
Q

telangiectasias are mostly seen in the

A

pons

218
Q

true or false: telangiectasias require no tx

A

true

219
Q

classic appearance include of an enlarged enhancing stellate venous complex extending to the ventricular or cortical surace

A

venous malformations

220
Q

thin-walled sinusoidal vessels (neither arteries nor vein) which may present with seizures or small parenchymal hemorrhages

A

cavernous malformations

221
Q

drugs that have been commonly associated with brain hemorrhage

A

amphetamines and cocaine

222
Q

cerebral amyloid angiopathy or congophilic angiopathy is associated with ____ 30% of cases

A

dementia

223
Q

evolution of blood products in benign IC hemorrhage

A

peripheral to central

224
Q

evolution of blood products in malignant IC hemorrhage

A

irregular and complex

225
Q

hemosiderin rim in benign IC hemorrhage

A

complete

226
Q

hemosiderin rim in malignant IC hemorrhage

A

delayed, incomplete

227
Q

surrounding edema appearance in benign IC hemorrhage

A

minimal/mild

228
Q

surrounding edema appearance in malignant IC hemorrhage

A

moderate/severe

229
Q

acute enhancement patterns in benign IC hemorrhage

A

minimal (unless AVM)

230
Q

acute enhancement patterns in malignant IC hemorrhage

A

moderate/severe

231
Q

most common brain tumors to hemorrhage

A

glioblastomas

232
Q

metastatic brain lesions prone to hemorrhage

A

bronchogenic CA, thyroid, melanoma, choriocarcinoma and renal cell carcinoma

Head and neck radiology (15 decks)

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