Nontraumatic Hemorrhage and Vascular Lesions Flashcards
(197 cards)
1
Q
What are the 4 segments of the aorta?
A
The ascending aorta, transverse aorta (mostly consisting of the aortic arch), aortic isthmus, and descending aorta.
2
Q
The “classic” AA with three “great vessels” originating separately from the arch is seen in 80% of cases. In 10-25%of cases, the left CCA shares a common V-shaped origin with the BCT (commonly referred to as a_______
A
“bovine arch,” a misnomer as this configuration bears no resemblance to the AA branching pattern seen in ruminants).
3
Q
Three thoracic aorta “lumps and bumps” are normal anatomic variants that should not be mistaken for pathology.
The __________is a narrowed segment just distal to the left SCA and proximal to the site of the fetal ductus
arteriosis.
An _______is a circumferential bulge in the aorta just beyond the ductus. Both the aortic isthmus and spindle typically disappear after two postnatal months but can persist into adulthood.
A _______is a focal bulge along the anteromedial aspect of theaortic isthmus and is seen in 10% of adults.
A
aortic isthmus
aortic spindle
ductus diverticulum
4
Q
The most common anomaly of the aortic arch?
A
The most common congenital arch anomaly—
seen in 0.5-1.0% of cases—is a left AA with an aberrant right SCA
5
Q
Where does an abberant SCA usually arise?
A
the aberrant right SCA arises from a dilated, diverticulum-like structure (Kommerell diverticulum)
6
Q
a _________branching is strongly associated with cyanotic congenital heart disease (98% prevalence).
A
right AA with mirror image
7
Q
The ___________provide the major blood supply to the face and cerebral hemispheres. It course superiorly, anteromedial to the internal jugular veins.
They terminate at about the C3-C4 or C4-C5
level by dividing into the internal and external carotid arteries
A
common carotid arteries (CCAs)
8
Q
The cervical internal carotid artery is entirely extracranial and is designated as the C1 segment.
In 90% of cases, the cervical ICA arises from the_______
A
CCA posterolateral to the external carotid artery.
9
Q
The C1 ICA has two parts, the carotid bulb and the ascending segment.
The _________is the most proximal aspect of the cervical ICA and is seen as a prominent focal dilatation with a cross-sectional area nearly twice as large as that of the distal ICA.
A
carotid bulb
10
Q
T or F
The ascending ICA segment courses cephalad in the carotid space, a fascially defined tubular sheath that contains all three layers of the deep cervical fascia. The cervical ICA has no normal branches in the neck.
A
T
11
Q
Anastomosis of the Ascending Phar A
A
Tympanic branch → petrous ICA
Several rami → cavernous ICA
Odontoid arch/musculospinal branches → VA
12
Q
Maxillar artery anastomoses
A
Vidian artery → petrous ICA
MMA → inferolateral trunk → cavernous ICA
Artery of foramen rotundum → inferolateral trunk → cavernous ICA
Middle/recurrent meningeal arteries → OA → intracranial ICA
Deep temporal → OA → intracranial ICA
13
Q
The most common imaging findings in extracranial ASVD are___________
A
mural calcifications, luminal irregularities, varying degrees of vessel stenosis, occlusion, and thrombosis
14
Q
CECT and CTA source images display the carotid lumen in cross section. ________________is
the most common finding in ASVD
A
Nonstenotic smooth luminal narrowing
15
Q
When ectasia occurs in the posterior circulation,
it is termed_________
A
“vertebrobasilar dolichoectasia” (
16
Q
Ectasias can involve any part of the intracranial circulation but are most common in the vertebrobasilar arteries
and________
A
supraclinoid ICA
17
Q
_________are focal arterial enlargements that are usually superimposed on an
ectatic artery. ASVD FAs are most common in the vertebrobasilar circulation. When they occur in the anterior
circulation, they can produce a rare but dramatic manifestation called a giant “serpentine” aneurysm
A
Atherosclerotic fusiform aneurysms (FAs)
18
Q
While CTA accurately depicts_______ of large intracranial arterial segments (cavernous and supraclinoid ICA, proximal MCA), lesser degrees of stenosis and ASVD in smaller second- or third-order branches are best depicted on DSA.
A
> 50% stenoses
19
Q
A _______________—defined as any lesion with an intracranial stenosis > 50% in the same vascular
distribution distal to a primary extracranial stenosis—is present in 20% of patients (10-27). Cumulative stroke
and/or death rate is higher than with either stenosis alone.
A
“tandem” stenosis
20
Q
The term __________is sometimes used by neurologists to designate the confluent WM lesions associated with
arteriolosclerosis, i.e., small vessel vascular disease. This is one of the most grossly visible markers that aging and
vascular risk factors inflict on the brain.
A
leukoariosis
21
Q
MR. Patchy or confluent periventricular and subcortical white matter hypointensities are seen on T1WI.
The lesions are hyperintense on T2WI and are especially prominent on FLAIR (10-31A). T2* (GRE, SWI) sequences often demonstrate multifocal “blooming” hypointensities, especially in the presence of chronic hypertension.
does not enhance on T1 C+ and does not demonstrate restricted diffusion on DWI.
What are these?
A
Arteriolosclerosis
22
Q
Ddx for arteriolosclerosis
A
is normal agerelated hyperintensities
enlarged perivascular (Virchow-Robin) spaces (PVSs
Demyelinating disease
23
Q
______________is an uncommon segmental nonatherosclerotic, noninflammatory disease of unknown
etiology that affects medium and large arteries in many areas of the body.
A
Fibromuscular dysplasia (FMD)
24
Q
Blood vessels involved in FMD
A
The cervicocephalic vessels are involved in up to 70% of cases
25
FMD carries an increased risk of developing _________ It is
present in approximately 7-10% of patients with cervical FMD
IC Aneurysm
26
The most common type of FMD
By far the most common type (type 1) is
medial fibroplasia, accounting for approximately 85% of all FMD cases. Here the media has alternating thin and
very thick areas formed by concentric rings of fibrous proliferations and smooth muscle hyperplasia
27
\_\_\_\_\_\_\_\_\_\_can present
with transient ischemia attack, bruit, stroke, or dissection (often with Horner syndrome, i.e., ptosis, pupil
constriction, facial anhidrosis).
Cervical FMD
28
Meds for FMD
antiplatelet therapy for asymptomatic individuals with cervical FMD.
Percutaneous balloon angioplasty is
recommended for patients with recent-onset or resistant hypertension, TIA, or stroke
29
In the past, \_\_\_\_\_\_\_\_was considered the gold standard for the diagnosis of FMD. However, CTA accurately depicts FMD in the cervicocephalic arteries and also allows visualization of the intracranial vessels to detect the presence of associated aneurysms
DSA
30
What is the problem with TOF MRA in FMD
TOF MRA is problematic because artifacts
caused by patient motion or in-plane flow and susceptibility gradients can mimic the appearance of FMD
31
Problem with duplex for FMD
Duplex
sonography and color Doppler can depict FMD only when the lesion is located proximally.
32
What type of FMD?
An irregular “corrugated” or “string of beads” appearance with alternating areas of constriction and dilatation that are wider than the original lumen is the typical appearance
Type 1
33
FMD
In \_\_\_\_\_\_\_\_\_\_\_\_, a smooth, longsegment tubular narrowing is present.
In\_\_\_\_\_\_\_\_\_\_ FMD, asymmetric diverticulum-like outpouchings from one side of the artery are present
type 2 (intimal fibroplasia)
type 3 (adventitial)
34
\_\_\_\_\_\_\_\_\_\_\_is an uncommon but important cause of ischemic stroke in young and
middle-aged adults. Timely therapy can reduce the immediate stroke risk and mitigate long-term sequelae of
craniocervical dissections, so imaging diagnosis is crucial to patient management.
Craniocervical arterial dissection (CAD)
35
A dissecting aneurysm is a dissection characterized by an outpouching that extends beyond the vessel wall.
Most occur with subadventitial dissections and are more accurately designated as \_\_\_\_\_\_\_\_\_(i.e., they lack
all normal vessel wall components).
pseudoaneurysms
36
Almost \_\_\_\_\_\_\_of extracranial dissections are “spontaneous,” i.e., nontraumatic. The remainder result from blunt or
penetrating injury. Most nontraumatic dissections occur secondary to an underlying vasculopathy such as FMD,
Marfan syndrome, or other connective tissue disorder (e.g., Ehlers-Danlos type 4).
60%
37
Dissections typically occur in the most mobile segment of a vessel, often starting or ending where the
vessel transitions from a relatively free position to a position fixed by an encasing bony canal.\_\_\_\_\_\_\_\_
is the most common overall site in the head and neck
The extracranial ICA
38
Sx of AD
Neck pain and headache are the most common symptoms. One or more lower cranial nerve palsies
including postganglionic Horner syndrome may occur. Pulsatile tinnitus is a less frequent presentation
39
Tx options for AD
Anticoagulation is the recommended treatment for extracranial arterial dissection.
Six months of antiplatelet therapy in asymptomatic patients with stable imaging findings is common
40
CT findings of AD
NECT may show crescent-shaped thickening caused by the wall hematoma.
41
Approximately \_\_\_\_\_\_of vertebral artery dissections cause posterior fossa subarachnoid hemorrhage
20%
42
MRI of Arterial dissection
## Footnote
T1WI with fat saturation is the best sequence for demonstrating CAD. A hyperintense crescent of subacute blood adjacent to a narrowed “flow void” in the patent lumen is typical (10-40). T2WI may show
laminated layers of thrombus that \_\_\_\_\_\_\_\_\_\_on T2\*
“blooms”
43
Extracranial ICA dissections typically spare the \_\_\_\_\_\_\_\_\_beginning two to three centimeters
distal to the bifurcation and terminating at the exocranial opening of the carotid canal (10-41).
Vertebral dissections are most common around the skull base and upper cervical spine.
carotid bulb,
44
In arterial dissection, The most common finding on DSA is a smooth or slightly irregular, tapered mid-cervical narrowing. CAD with occlusion shows a flame-shaped\_\_\_\_\_\_
“rat-tail” termination
45
Vasospasm with multifocal intracranial foci of arterial constriction and dilation is a common, well-recognized
complication of \_\_\_\_\_\_and is the most common cause of severe vasoconstriction
aneurysmal subarachnoid hemorrhage (aSAH)
46
\_\_\_\_\_\_\_\_\_\_\_also known as Call-Fleming syndrome) is associated with nonaneurysmal subarachnoid hemorrhage, pregnancy, and exposure to certain drugs.
The diagnosis requires demonstration of multifocal segmental arterial constrictions that resolve, then recur
Reversible cerebral vasoconstriction syndrome,
47
Involvement of the cortex/subcortical white matter together with the basal ganglia (BG) is strongly suggestive of \_\_\_\_\_\_\_
T1 scans can be normal or show multifocal cortical/subcortical and BG hypointensities.
T2/FLAIR scans demonstrate hyperintensities in the same areas (10-50A). T2\* (GRE, SWI) may show parenchymal
microhemorrhages and/or SAH in some cases
vasculitis.
48
\_\_\_\_\_\_\_\_\_\_is an idiopathic progressive arteriopathy characterized by stenosis of the distal (supraclinoid) ICAs and formation of an abnormal vascular network at the base of the brain
Moyamoya disease (MMD) i
49
The pathophysiology of MMD has been extensively investigated but remains poorly understood. Genetic,
acquired, and environmental factors have all been implicated. Aberrant expression of \_\_\_\_\_and \_\_\_\_proteins in
the walls of MMD vessels has been demonstrated, but its significance is uncertain
IgG and S100 A4
50
Diseases associated with Moya Moya
The disease is also associated with several genetically
transmitted disorders including neurofibromatosis type 1, trisomy 21 (Down syndrome), and a spectrum of
hemoglobinopathies such as sickle cell anemia
51
The clinical features of MMD in children differ from those in adults. When MMD presents in childhood, the initial
symptoms are usually \_\_\_\_\_\_In adults, approximately half of all patients develop\_\_\_\_\_\_ from
rupture of the fragile moyamoya collateral vessels. The
ischemic.
intracranial hemorrhage
52
Multiple enhancing punctate\_\_\_\_\_\_ or \_\_\_\_\_\_\_(MR) in the basal ganglia are the most striking
findings in MMD.
T1 and T2 scans show markedly narrowed ________ with multiple tortuous, serpentine “flow voids”
The appearance of multiple tiny collateral vessels in enlarged CSF spaces has been likened to “\_\_\_\_\_\_
“dots” (CECT) or “flow voids”
Supraclinoid ICAs
swimming worms in a bare cistern.”
53
In MOYA MOYA
An \_\_\_\_\_\_sign with sulcal hyperintensity from slow flow in leptomeningeal collaterals is sometimes seen on FLAIR
and correlates with decreased vascular reserve in the affected hemisphere.
“ivy”
54
IN MOYA MOYA
Multiple microbleeds can be detected on T2\* GRE scans in 15-40% of patients and are associated with increased risk
of overt cerebral hemorrhage. Susceptibility-weighted imaging (SWI) shows increased conspicuity of deep
medullary veins, an appearance dubbed the \_\_\_\_\_\_\_sign.
“brush”
55
DSA, CTA, and MRA show predominantly anterior circulation disease with marked narrowing of both supraclinoid ICAs\_\_\_\_\_\_\_
(“bottle neck” sign).
56
Prominent deep-seated lenticulostriate and
thalamoperforator collaterals are present, forming the\_\_\_\_\_\_\_\_ appearance characteristic of moyamoya.
“puff of smoke”
57
The differential diagnosis of idiopathic (“true”) moyamoya disease includes other slowly developing occlusive vasculopathies INCLUDING?
Radiation therapy, neurofibromatosis type 1 (NF1), trisomy 21, sickle cell disease, and even atherosclerosis may develop multiple small moyamoya-like collateral vessels.
58
A unilateral “\_\_\_\_ is a rare nonprogressive congenital anomaly that should be differentiated from
MMD
aplastic” or twig-like M1 MCA
59
CADASIL is caused by highly stereotyped missense point mutations in the\_\_\_\_\_\_ gene
NOTCH3 gene.
60
IN CADASIL
Bilateral, multifocal T2 and FLAIR hyperintensities in the periventricular and deep WM begin to appear by age 20.
Although these findings are nonspecific, involvement of the _______ AND \_\_\_\_\_\_\_\_\_\_\_\_has high
sensitivity and specificity in differentiating CADASIL from the much more common sporadic cerebral small vessel
diseas
anterior temporal lobe and external capsule
61
Uncommon manifestations of CNS amyloid disease include a focal, tumefactive mass-like lesion called an
\_\_\_\_\_\_\_\_
amyloidoma
62
Rarely, cerebral amyloid disease presents as an \_\_\_\_\_\_\_\_\_\_\_\_\_with diffuse
inflammatory changes that primarily affect the white matter
amyloid β-related angiitis (ABRA)
63
Aβ42 is principally found in \_\_\_\_\_\_whereas the shorter, relatively more soluble Aβ40 is the major form found in\_\_\_\_\_\_\_\_\_\_
AD-associated neuritic plaques
CAA.
64
Failure to clear Aβ from the brain has two major consequences:
(1) intracranial hemorrhages associated with rupture of Aβ-laden vessels in CAA and
(2) altered neuronal function caused by pathologic accumulation of Aβ and other soluble metabolites in AD.
65
Enhancement on CECT is rare in cerebral amyloid disease and occurs only if a focal mass OR _______ is present
(“amyloidoma”) or ABRA is present.
66
WHAT ARE THE 4 VARIANTS OF THE BRACHIO
CEPHALIC TRUNK
Four arch variants are depicted:
Brachiocephalic trunk (BCT) and R ICA arising from V-shaped common origin ,
L ICA arising from BCT ,
L VA arising directly from arch ,
aberrant R SCA arising from arch as fourth “great vessel
67
WHAT ANASTOMOSES ARE SHOWN?
Graphic shows numerous anastomoses between the ECA and cavernous ICA, including via the artery of
the foramen rotundum , lateral mainstem artery , and ophthalmic artery
68
WHAT ARTERY HAS BEEN AFFECTED?
Section through the midbrain in the same case shows an old midline penetrating artery infarction , possibly secondary to an artery of Percheron occlusion. 10-7D. More cephalad section through the inferior third ventricle shows a subacute inferomedial thalamic infarct , consistent with artery of Percheron occlusion
69
WHAT IS SHOWN IN THIS CEA SPECIMEN?
Carotid endarterectomy specimen shows ulcerated intima , calcification , intraplaque hemorrhage
70
What is shown in this CTA?
Axial CTA source image shows irregular, ulcerated atherosclerotic plaque along the aortic arch,
proximal descending thoracic aorta.
71
What is shown in this case of ICA stenosis?
(Left) DSA shows critical ICA stenosis . (Right) MRA in the same case shows a “flow gap”
characteristic of a highgrade flow-limiting lesion.
72
What sign is shown?
(Left) DSA shows ulcerated plaque causing high-grade, near-total stenosis with a “string”
sign . (Right) Late phase shows the distal cervical ICA . Filling defects are caused by thrombus.
73
What is shown?
MP-RAGE shows intraplaque hemorrhage with tiny residual lumen in the right ICA,
subintimal hemorrhage in the left ICA
74
What is your dx?
Longitudinal color Doppler ultrasound shows highgrade ICA stenosis. The arterial lumen is
significantly narrowed with “aliasing” flow artifact due to increased flow velocity.
75
WHAT VALUES ARE INCREASED IN THIS CASE OF STENOSIS?
Spectral Doppler analysis in the same case shows findings of stenosis. Both PSV and EDV are
markedly increased, consistent with stenosis \> 70
76
WHAT PHENOMENON IS SHOWN?
Longitudinal color Doppler US shows mild subclavian steal with arm resting.
77
WHAT ARE SHOWN?
Sagittal T1WI in an elderly man without hypertension or dementia
Sagittal T1WI in an elderly man without hypertension or dementia shows an extremely elongated “flow void” of the basilar artery . The dolichoectatic artery indents and elevates the third ventricle , which appears compressed and draped over the basilar bifurcation.
10-24B. Coronal T1 C+ scan in the same case shows slow flow with enhancement in the ectatic basilar artery . Note that the third ventricle is elevated, compressed by the VBD.
78
WHAT ARE SHOWN?
Autopsy case demonstrates ASVD fusiform ectasias of the ICAs and MCAs . The posterior (vertebrobasilar) circulation is relatively spared .
Autopsy case shows extreme ectasia of the horizontal MCA segment
79
WHAT TYPE OF STENOSIS IS SHOWN?
Lateral DSA shows high-grade narrowing of the cervical ICA , small distal ICA (from reduced flow), “tandem” stenosis
80
WHAT TYPE OF STENOSIS IS SHOWN?
Lateral DSA shows high-grade narrowing of the cervical ICA , small distal ICA (from reduced flow), “tandem” stenosis
81
WHAT ARTERIES ARE AFFECTED?
(Left) AP, (right) lateral DSA show extensive changes of ASVD in the vertebrobasilar artery ,
proximal right PCA , PICA
82
WHAT ARE SHOWN?
Magnified lateral DSA shows severe intracranial ASVD with numerous foci of irregular narrowing and
dilatation in distal MCA branches mimicking vasculitis
83
WHAT IS SHOWN?
Axial FLAIR scan in an elderly demented patient with chronic hypertension and small vessel vascular disease shows volume loss, confluent periventricular WM hyperintensities , and multiple lacunar
infarcts
84
WHAT SEQUENCE IS SHOWN?
T2\* GRE scan in the same patient shows multifocal hypointensities characteristic of cerebral
microbleeds , old hypertensive basal ganglia hemorrhage
85
GRAPHIC REPRESENTATION OF WHAT DSE?
Graphic of the carotid bifurcation shows the principal subtypes of FMD. Type 1 appears as alternating areas of constriction and dilatation , type 2 as tubular stenosis , and type 3 as focal corrugations ± diverticulum
86
WHAT ARE SHOWN IN THIS CASE OF TYPE 1 FMD?
AP DSA shows type 1 FMD in both ICAs with sparing of the bulbs , “string of beads” in midcervical
segments , small unruptured saccular aneurysm of the right supraclinoid ICA.
87
What type of FMD?
(L) DSA of internal carotid, (R) vertebral arteries with type 3 FMD shows diverticulum-like outpouchings , saccular aneurysm
88
Describe the pathophysion of arterial disseaction?
Extracranial ICA dissection shows intimal tear , subintimal thrombus compressing the
residual lumen . The bulb is spared
89
What is your dx?
Two axial sections show carotid dissection with subintimal hematoma , compressed residual lumen
90
What sign is shown?
DSA in 2 cases of cervical ICA dissection. (Left) Classic “rat-tail” narrowing of the mid carotid with sparing of the bulb. (Right) Upper ICA dissection terminates at the exocranial opening of the bony
carotid canal
91
T1WI in a 28-year-old woman with Marfan syndrome and a 4-day history of neck pain
dissection of both cervical internal carotid arteries , both vertebral arteries . Mural thrombus surrounds tiny residual “flow voids” in all 4 vessels. 10-42B. T2\* GRE in the same patient demonstrates that the mural thrombus around the distal cervical ICAs “blooms”
92
What artery could have been dissected?
CTA in a patient with supraclinoid ICA dissection shows hyperdense clot surrounding a very
narrow distal ICA . 10-44B. DWI in the same patient shows a focal acute infarct in the posterior limb of
the right internal capsule caused by embolization from the supraclinoid ICA dissection.
93
AP vertebral DSA in a 41-year-old woman with “thunderclap” headache shows multiple areas of
vasoconstriction and dilatation. 10-45B. Repeat vertebral DSA 2 weeks later shows almost complete
resolution.
Reversible cerebral vasoconstriction syndrome
94
What is shown in this pt with DSA done post partum?
Common carotid angiogram, lateral view, in a 28-year-old postpartum woman shows multifocal
“beaded” areas of alternating stenoses and dilatations , characteristic of vasculitis.
10-46B. Vertebral angiogram, AP view, in the same patient shows multiple “beaded” foci in the posterior circulation as
well. Postpartum angiopathy.
95
Axial FLAIR scan in a patient with a history of recent streptococcal meningitis
shows several hyperintense foci in the basal ganglia and thalami .
10-50B. DWI in the same patient shows multiple foci of restricted diffusion in the basal ganglia. Other images (not shown) demonstrated peripheral lesions in the cortex and subcortical white matter. Findings suggest infarcts secondary to meningitic vasculitis.
96
Look at the calvaria and clivus. What is your dx?
Sagittal T1WI in a 29-year-old woman with sickle cell disease (SCD) shows thick calvaria with
hypointense hematopoietic marrow . The clivus and cervical vertebral bodies are also
hypointense. The intervertebral discs appear “brighter” than the vertebral bodies. 10-51B. FLAIR scan in
the same patient shows punctate hyperintensities in both watershed zones , a common finding in SCD.
97
What is your diagnosis?
MMD in a 3-year-old shows near-total supraclinoid ICA stenosis with innumerable tortuous enlarged moyamoya-like collaterals
98
What arteries form collaterals in this fig?
Vertebral angiogram in the same patient shows moyamoya-like collaterals from enlarged
thalamoperforating arteries
99
What are shown and what is the dx?
T1WI in the same patient shows multiple “flow voids” from enlarged moyamoya collaterals in the
basal ganglia, thalami
100
What is your dx?
FLAIR scan through the basal ganglia shows external capsule lesions , highly suggestive of
CADASIL
101
What is shown?
FLAIR scan in the same patient shows anterior temporal lobe WM hyperintensities . NOTCH3
mutation confirmed CADASIL.
102
a 30-year-old man with fever, oral ulcers, and bilateral upper extremity weakness. Patient has this MRI. What is your dx?
Axial T1 C+ FS scan in the same patient shows that the pontine mass enhances moderately but
heterogeneously. 10-58D. T1 C+ FS scan shows a ringenhancing lesion in the right caudate nucleus and
anterior limb of the internal capsule . Biopsy-proven Behçet disease
103
Pt has lupus. What is your dx?
Coronal T1 C+ scan in the same patient shows mild punctate and linear foci of enhancement in the
subcortical and deep cerebral WM . 10-60D. Coronal T1 C+ shows patchy and linear enhancing foci in the subcortical WM . Note the burr hole from biopsy. Histopathologic examination disclosed CNS
lupus vasculitis.
104
What type of imaging?
DTI trace image in the same patient shows acute restriction in the anterior division of the right
middle cerebral artery
105
This figure is consistent with?
Acute hematoma with a fluid level ; microbleeds and old lobar hemorrhages are also typical findings in cerebral amyloid disease
106
This scan is typical of?
Scans in a patient with headache and CAA show convexal SAH , confluent WM lesions , superficial siderosis , and microbleeds
107
What sign is shown in this pt with CAA
Scans in a patient with headache and CAA show convexal SAH , confluent WM lesions , superficial siderosis , and microbleeds
108
What is your dx?
T2\* SWI scan through the upper ventricles shows innumerable peripheral “blooming black dots” in
both hemispheres as well as the superficial siderosis characteristic of cerebral amyloid angiopathy.
10-67F. T2\* SWI through the corona radiata shows additional areas of siderosis and microhemorrhages
. Because of the clinical findings plus cerebral edema and mass effect, this case represents CAA-related
inflammation (ABRA).
109
What are shown in this pt with HUS?
T2\* SWI scan in the same patient shows multiple “blooming black dots” in the deep cerebral WM of
both hemispheres . 10-75D. More cephalad SWI scan in the same patient shows more “blooming” foci in
the corona radiata
110
What is your dx?
NECT scan shows spontaneous nontraumatic subacute combined epi- and subdural hematoma
associated with a focal calvarial lesion
111
T or F
Hematomas consist of two distinct regions: A central core and a peripheral rim or boundary. In general, hemoglobin
degradation begins in the clot periphery and progresses centrally toward the core.
T
112
What stage of hemorrhage?
a loose fibrin clot that contains plasma, platelets, and intact red blood cells is formed. At this stage, diamagnetic intracellular oxyhemoglobin predominates in the hematoma.
HYPERACUTE HEMORRHAGE. Hyperacute hemorrhage is minutes to under 24 hours old
113
What stage of clot?
## Footnote
Profound hypoxia within the center of the clot induces the transformation of oxy-Hgb to deoxy-Hgb. Iron in deoxy-Hgb is paramagnetic because it has four unpaired electrons.
ACUTE HEMORRHAGE. Acute ICH is defined as between one to three days old.
114
What stage?
Hemoglobin remains contained within intact RBCs. Hemoglobin at the hypoxic center of the clot persists as deoxy-Hgb. The periphery of the clot ages more rapidly and therefore contains intracellular met-Hgb. Intracellular met-Hgb is highly paramagnetic, but the intact RBC membrane prevents direct dipole-dipole
interactions.
EARLY SUBACUTE HEMORRHAGE. Early subacute hemorrhage is defined as a clot that is from three days to one
week old
115
What stage?
As RBCs lyse, met-Hgb becomes extracellular. Met-Hgb is now exposed directly to plasma water, reducing T1 relaxation time and prolonging the T2 relaxation time.
LATE SUBACUTE HEMORRHAGE. Late subacute hemorrhage lasts from one to several weeks.
116
What stage of stroke?
Heme proteins are
phagocytized and stored as ferritin in macrophages. If the capacity to store ferritin is exceeded, excess iron is
stored as hemosiderin. Intracellular ferritin and hemosiderin induce strong magnetic susceptibility
CHRONIC HEMORRHAGE
117
Patients with unexplained or atypical sICH on NECT may benefit from \_\_\_\_\_\_\_, which can help distinguish between tumor bleeding and nonneoplastic (“pure”) hemorrhage.
dual-energy CT
118
The most common cause of spontaneous ICH in infants less than 34 gestational weeks is\_\_\_\_\_\_\_
germinal matrix hemorrhage.
119
The most common nontraumatic cause of spontaneous intraventricular hemorrhage (IVH) in neonates beyond 34
gestational weeks is\_\_\_\_\_\_\_\_
dural venous sinus thrombosis
120
The most common cause of sICH in children ages one to 18 years is an underlying\_\_\_\_\_\_\_\_\_
vascular malformation
121
An underlying vascular malformation is the most common cause of sICH in young adults as well (5-14).\_\_\_\_\_\_\_\_\_\_
is the second most common cause of unexplained hemorrhage
Drug abuse
122
Multifocal brain bleeds that occur at all ages include:
venous thrombosis , PRES , vasculitis (especially
fungal), septic emboli, thrombotic microangiopathy, and acute hemorrhagic leukoencephalopathy.
123
Generalized arteriosclerosis with lipohyalinosis and fibrinoid necrosis is common in patients with hICH. In some cases, \_\_\_\_\_\_\_in the basal ganglia can be identified
small fibrosed pseudoaneurysms
124
In the presence of \_\_\_\_\_\_\_\_\_\_\_\_\_the
hemorrhage may appear inhomogeneously hyperdense with lower density areas and even fluid-fluid levels
active bleeding or coagulopathy,
125
Most hICHs are avascular on CTA (5-26B). However, an enhancing \_\_\_\_\_\_\_\_with contrast extravasation can sometimes be identified in actively bleeding lesions.
“spot” sign
126
MR is the most sensitive study to detect\_\_\_\_\_\_\_. The vast majority of patients have multifocal and confluent areas of
white matter hyperintensity on T2/FLAIR scans. At least one-third have evidence of old lobar or petechial
microhemorrhages, seen as multifocal “blooming black dots” on T2\* (GRE, SWI)
CAA
127
The etiology of RCH is most likely CSF\_\_\_\_\_\_\_ with inferior displacement or “sagging” of the cerebellar
hemispheres. Tearing or occlusion of bridging tentorial veins is thought to result in superficial cerebellar
hemorrhage, with or without hemorrhagic necrosis.
hypovolemia,
128
\_\_\_\_\_\_\_\_\_\_\_\_represent perivascular collections of hemosiderin-containing macrophages. They
indicate prior bleeds from an underlying hemorrhage-prone microangiopathy.
Cerebral microbleeds (CMBs)
129
Ddx of CMB
Diffuse axonal/vascular injury
Cerebral amyloid angiopathy
o Apolipoprotein E4 polymorphism
Chronic hypertensive encephalopathy
Hemorrhagic metastases
130
NONHEMORRHAGIC CAUSES OF “BLOOMING BLACK DOTS” ON T2\*
Common
• Pneumocephalus
Less Common
Multiple parenchymal calcifications
o Neurocysticercosis
o Tuberculomas
131
Describe the Hb content of the ff bleeds at different stages?
(A) Hyperacute hemorrhage is a water-rich clot that is 95-98% oxy-Hgb.
(B) Acute hemorrhage contains mostly oxy-Hgb. Some RBCs in the intensely hypoxic clot center may contain deoxy-Hgb.
(C) Early subacute clots contain deoxy-Hgb in the center, intracellular met-Hgb in the periphery.
(D) Late subacute clots contain mostly extracellular met-Hgb.
(E) Chronic clots contain a yellowish pool of extracellular met-Hgb surrounded by a hemosiderin rim.
(F) Only a slit-like scar remains.
132
What is your dx?
T2WI shows that the clot is heterogeneously hyperintense and is surrounded by hyperintense vasogenic edema . 5-4D.
T2\* GRE scan shows “blooming” around the periphery of the clot . Tubular hypointensity in adjacent cortical veins suggests venous thrombosis
133
What is the age of the ICH?
What is the dx?
T1WI obtained 4 days following ictus in a young patient with a spontaneous parenchymal ICH. The clot
is mostly hyperintense .
5-5B. The clot is profoundly hypointense on T2WI. The T1-T2 “bright-dark” appearance is consistent with late acute/early subacute hemorrhage. DSA (not shown) disclosed a mostly thrombosed arteriovenous malformation
134
What is the age of the ICH in the MRI shown?
Gross autopsy case shows residua of remote striatocapsular hemorrhage.
A slit-like cavity with a small amount of yellowish fluid is surrounded by dark hemosiderin staining . Note volume loss with enlarged right frontal horn , gliotic brain surrounding old hematoma. (Courtesy R. Hewlett, MD.)
5-9A. Sagittal T1WI in a patient 2 years following hypertensive hemorrhage shows ovoid hyperintense cavity
135
Axial T1WI in a 34-week premature infant with sepsis. What is the dx?
Axial T1WI in a 34-week premature infant with sepsis shows hyperintense clot in the third and
lateral ventricles as well as thrombus in the straight sinus and torcular herophili . 5-10B. T2WI
in the same patient shows the very hypointense acute blood within the ventricles as well as an
enlarged, thrombosed straight sinus and venous sinus confluence
136
What sign is shown?
Coronal T2\* GRE scan shows “blooming” clot in both lateral ventricles and the fourth ventricle . The superior sagittal sinus and straight sinus are thrombosed. 5-10D. Coronal T1 C+ scan shows the classic “empty delta” sign of dural sinus thrombosis in the superior sagittal and straight sinuses . In
a term or near-term infant, dural venous sinus occlusion is the most common cause of intraventricular
hemorrhage.
137
What could this be in a child?
NECT scan in a child with a family history of multiple cavernous malformations shows a small,
solitary, calcified lesion in the right cerebral hemisphere . 5-11B. Several weeks later, the child
experienced sudden onset of severe headache and left-sided weakness. Acute rebleeding into the underlying
cavernous malformation has produced a large parenchymal hematom
138
NECT scan in a young adult female with sudden severe headache followed by coma with no history of
hypertension, drug abuse, or other predisposing factors
Both lateral ventricles are filled with acute clot . 5-14B. Lateral selective internal carotid DSA in the same patient shows a tangle of vessels in the cingulate gyrus with an “early draining vein” and a contrast meniscus around a filling defect . AVM
with hemorrhage caused by draining vein occlusion
139
140
What sinus could be thrombosed
NECT scan in a 23 yo woman with headaches shows left temporoparietal hemorrhage . CTV
demonstrated occluded TS, vein of Labbé
141
What is shown?
Bilateral remote cerebellar hemorrhage following resection of a supratentorial neoplasm. (Top) T2\* GRE shows bilateral “blooming” lesions . (Bottom) DWI shows some restriction in the right acute
hemorrhage
142
Intracranial aneurysms are classified by their gross appearance. \_\_\_\_\_\_\_\_\_\_aneurysms are the most
common type and typically arise eccentrically at vessel branch points
Saccular or “berry”
143
\_\_\_\_\_\_\_\_\_often resemble
“true” saccular aneurysms (SAs) in shape but are contained by cavitated clot, not components of arterial walls.
Pseudoaneurysms
144
\_\_\_\_\_\_\_are thin-walled hemispheric bulges that—as the name suggests—resemble cutaneous
blood blisters in appearance
Blood blister-like aneurysms
145
LOCATION. Because most saccular aneurysms arise from the circle of Willis (COW) or the middle cerebral artery
(MCA) bifurcation, the most common locations for aneurysmal SAH are the\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_
suprasellar cistern and sylvian fissures
146
Acute aSAH is \_\_\_\_\_\_\_\_with brain on T1WI. The CSF cisterns may appear smudged or “dirty.” Because aSAH is hyperintense to brain on T2WI, it may be difficult to identify
isointense
147
CTA is positive in \_\_\_\_\_\_\_of aSAH cases if the “culprit” aneurysm is two millimeters or larger (6-5B).
While DSA is still considered the gold standard for detecting and delineating aneurysm angioarchitecture, many patients with aSAH and positive CTA undergo surgical clipping without DSA.
95%
148
\_\_\_\_\_\_\_\_is much more limited than aSAH and is localized to the interpeduncular, ambient, and prepontine cisterns. Occasionally, pnSAH spreads into the posterior aspect of the suprasellar cistern. It rarely extends into the sylvian fissures
Perimesencephalic nonaneurysmal SAH (pnSAH)
149
\_\_\_\_\_\_\_\_\_\_\_\_on MR is a nonspecific imaging finding and does not always denote subarachnoid hemorrhage. In addition to aSAH, FLAIR hyperintense CSF often occurs with flow disturbances and technical artifacts such as incomplete CSF nulling.
Sulcal-cisternal FLAIR hyperintensity
150
\_\_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_
have all been implicated in the pathogenesis of post-SAH DCI.
Microcirculatory dysfunction related to endothelial damage, microvascular thrombosis, and loss of autoregulation
151
\_\_\_\_\_\_\_\_is an intraocular hemorrhage that is found in 12-13% of patients with aSAH. TS is associated with more severe SAH grades and is probably caused by a rapid increase in intracranial pressure (ICP). The
hemorrhage can be subhyaloid (most common), retinal, or vitreous
Terson syndrome (TS)
152
Where is the location of the aneurysm?
right ICA angiogram in the same patient shows a large trilobed IC-PCoA aneurysm
153
WHAT DOES THE ARROW SHOW?
AP vertebral DSA shows severe vasospasm from ruptured anterior circulation aneurysm. Distal
vessels are barely opacified
154
What is your diagnosis?
Series of MR images shows typical findings of superficial siderosis in a patient with bilateral
sensorineural hearing loss and progressive ataxia. FSE T2WI shows linear hypointensity around the surfaces
of the pons, cerebellum . T2\* GRE scans show marked “blooming” covering the pons and cerebellar
hemispheres, extending into and along the folia
155
Where is the aneurysm?
CTA shows an intensely enhancing saccular aneurysm at the MCA bi-/trifurcation just anterior to
the temporal lobe hematoma. 6-24D. Coronal MIP of the CTA nicely demonstrates the aneurysm . The
M1 MCA segment is elevated by the mass effect from the hematoma
156
Where is the aneurysm?
Coronal MIP of the CTA in the same patient shows a patent saccular aneurysm at the terminal
bifurcation of the left ICA.
157
WHAT IS SHOWN?
Lateral DSA shows the aneurysm together with a classic “Neptune's trident” appearance of a persistent trigeminal artery
158
WHAT TYPE OF ANEURYSM IS SHOWN?
NECT scan shows typical features of a giant saccular aneurysm with extensive calcified mural
thrombus surrounding an isodense central clot. 6-28B. T1WI in the same patient shows concentric rings
of organized clot at different stages of evolution. The peripheral layer is hyperintense and older
whereas the more central irregular isointense clot is more recent. A small “flow void” represents
the residual patent lumen of the aneurysm.
159
Most \_\_\_\_\_\_\_\_\_\_are congenital lesions and represent morphogenetic errors affecting arteries, capillaries, veins, or a combination of these elements
CAVERNOUS MALFORMATIONS
160
CVMs have been traditionally classified by histopathology into four major types:
(1) arteriovenous malformations (AVMs),
(2) venous angiomas (developmental venous anomalies), (3) capillary telangiectasias (sometimes simply termed “telangiectasia” or “telangiectasis”), and
(4) cavernous malformations
161
Nonshunting CVMs include:
developmental
venous anomalies, capillary telangiectasias, and cavernous malformations.
162
CVMs that display arteriovenous shunting,\_\_\_\_\_ and \_\_\_\_\_\_\_
i.e., AVMs and arteriovenous fistulas (AVFs).
163
\_\_\_\_\_\_\_\_\_\_\_is a tightly packed “snarl” of thin-walled vessels with direct arterial to
venous shunting. There is no intervening capillary bed
An arteriovenous malformation (AVM)
164
Endothelial cells in cerebral AVMs express
1.
2.
3
This results in “downstream” derangements in vascular function and integrity
GLUT1 (a protein in the embryonic microvasculature),
matrix metalloproteinases (MMPs), proangiogenic growth factors such as vascular endothelial growth factor (VEGF).
165
Recent studies suggest that genetic factors affect both susceptibility and disease progression.
\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_have been
associated with both increased risk of developing a BAVM and frequency of hemorrhage.
Transforming growth factor β (TGF-β) and functionally active polymorphisms of the IL-1 complex
166
Multiple AVMs are almost always syndromic. Common associations include \_\_\_\_\_\_\_and segmental neurovascular
syndromes called \_\_\_\_\_\_\_\_\_\_\_\_\_Here somatic mutations of the neural crest occur along predefined migration paths, resulting in specific combinations of facial and intracranial vascular
malformations
hereditary hemorrhagic telangiectasia (HHT, also known as Rendu-Osler-Weber disease)
cerebrofacial arteriovenous metameric syndrome (CAMS).
167
\_\_\_\_\_\_\_\_in which AVMs are found in both the retina and brain, is one example of
a CAMS.
Wyburn-Mason syndrome,
168
T or F
Over 85% of AVMs are supratentorial, located in the cerebral hemispheres. Only 15% are found in the
posterior fossa.
T
169
AVMs are complex networks of abnormal vascular channels consisting of three distinct
components:
(1) feeding arteries, (2) a central nidus, and (3) draining veins
170
MRI findings of AVM
Because most AVMs are high-flow lesions, spins rapidly pass through the lesion and do not receive a refocusing
pulse. This produces the appearance of a tightly packed mass or a _______ or \_\_\_\_\_\_\_\_on both T1- and T2
scans
“honeycomb” of “flow voids”
171
The \_\_\_\_\_\_\_\_that supply an AVM are often enlarged and tortuous Flow-related angiopathy may be present, ranging from simple dilatation to endothelial thickening, stenosis, and occasionally even thrombosis and occlusion. A flow-induced “pedicle” aneurysm is seen in 10-15% of cases.
feeding arteries
172
The \_\_\_\_\_\_\_\_, the core of the AVM, is a tightly packed tangle of abnormal arteries and veins without an intervening
capillary bed. Up to 50% contain at least one aneurysmally dilated vessel (“intranidal aneurysm”).
nidus
173
\_\_\_\_\_\_\_\_\_\_typically opacify in the mid- to late-arterial phase (“early draining” veins). Veins draining AVMs are typically enlarged, tortuous, and may become so prominent that they form varices and exert local mass effect on the
adjacent cortex
Draining veins
174
\_\_\_\_\_\_\_\_\_\_\_\_is a rare entity characterized by diffuse angiogenesis and progressive hypervascular shunting
Cerebral proliferative angiopathy (CPA)
175
seen on MR as a large (usually more than six centimeters), diffusely dispersed network of innumerable dilated vascular spaces intermingled with normal brain parenchyma. Dense enhancement following contrast is
typical.
CPA
176
The major differential diagnosis of CPA is classic brain \_\_\_\_\_\_\_\_The absence of a dominant circumscribed nidus and
the presence of brain parenchyma interspersed between the abnormal vascular channels are distinguishing features
of CPA.
AVM.
177
\_\_\_\_\_\_\_also known as a dural arteriovenous shunt, is a network of tiny, crack-like vessels that shunt blood
between meningeal arteries and small venules within the wall of a dural venous sinus.
A dAVF,
178
Mechanism of DAVF formation
local hypoperfusion in a thrombosed dural venous sinus that results in elevated intrasinus pressure is the most commonly cited mechanism.
Upregulated angiogenesis within the dural sinus wall occurs after thrombosis and is considered the most likely etiology
179
While dAVFs can involve any dural venous sinus, the most common locations in adults are the _________ The superior sagittal sinus is a more common site in children
transverse, sigmoid, and cavernous sinuses.
180
\_\_\_\_\_\_of dural and transosseous feeders is usually required to identify arterial feeders, define the exact
fistula site, delineate venous drainage, and identify feeding artery or remote aneurysm of DVAF
DSA with superselective
catheterization
181
What is Cognard Classification for DAVF
Grade 1: In sinus wall; normal antegrade venous drainage (low risk; benign clinical course)
Grade 2A: In sinus; reflux to sinus, not cortical veins
Grade 2B: Reflux (retrograde drainage) into cortical veins (10-20% hemorrhage)
Grade 3: Direct cortical venous drainage; no venous ectasia (40% hemorrhage)
Grade 4: Direct cortical venous drainage + venous ectasia (65% hemorrhage)
Grade 5: Spinal perimedullary venous drainage
182
Bognard classification of DAVF
Type I: Dural arterial supply with antegrade drainage into venous sinus
o Type Ia: Simple dAVF with single meningeal arterial supply
o Type Ib: Complex dAVF with multiple meningeal arteries
Type II: Dural supply + ↑ intrasinus pressure → antegrade sinus, retrograde cortical venous drainage
Type III: Dural arteries drain into cortical veins
183
\_\_\_\_\_\_\_are typically high-flow lesions that result from rupture of the cavernous internal carotid artery (ICA)
directly into the cavernous sinus (CS), with or without a preexisting ICA aneurysm.
\_\_\_\_\_\_CCFs are usually slow-flow, low-pressure lesions that represent an arteriovenous fistula between dural branches of the cavernous
ICA and the cavernous sinus
“Direct” CCFs
“Indirect”
184
Most direct CCFs are traumatic, usually secondary to\_\_\_\_\_\_
central skull base fractures
185
Indirect CCFs are nontraumatic lesions and are thought to be degenerative in origin. In contrast to dAVFs
elsewhere, indirect CCFs rarely occur as sequelae of\_\_\_\_\_\_
dural sinus thrombosis
186
BARROW CLASSIFICATION OF CAROTID-CAVERNOUS FISTULAS
Type A: Direct ICA-cavernous sinus high-flow shunt
Type B: Dural ICA branches-cavernous sinus shunt
Type C: Dural ECA-cavernous sinus shunt
Type D: Both ICA/ECA dural branches shunt to CS
187
Tx options for direct CCF
The primary goal in treating a direct CCF is fistula closure, typically by transarterialtransfistula
detachable balloon embolization. Transvenous embolization via the internal jugular vein and inferior
petrosal sinus is another option.
188
Indirect CCFs often have multiple dural feeders from \_\_\_\_\_\_\_\_\_\_\_\_\_\_as well as deep branches of the ECA (middle meningeal and distal maxillary branches).
cavernous branches of the ICA (meningohypophyseal and
inferolateral trunks)
189
A\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ is a rare vascular malformation that usually consists of a single dilated pial
artery connecting directly to an enlarged cortical draining vein (7-20). No intervening capillary bed or nidus is
present.
pial arteriovenous fistula (pAVF)
190
\_\_\_\_\_\_\_\_\_\_\_is essentially a direct arteriovenous fistula between deep choroidal arteries and a persistent embryonic precursor of the vein of Galen
Vein of Galen Aneurysmal Malformation
191
In normal fetal development, arterial supply to the choroid plexus drains via a single
transient midline vein, the\_\_\_\_\_\_\_\_\_
median prosencephalic vein of Markowski
192
Imaging of VGAM
A large, rounded venous pouch drains into a persistent falcine sinus or prominent straight
sinus. The venous sinus confluence is often markedly enlarged.
193
\_\_\_\_\_\_\_\_\_\_\_), also called venous “angioma” or “venous malformation,” is an umbrellashaped
congenital cerebral vascular malformation composed of angiogenically mature venous elements. Dilated,
thin-walled venous channels lie within (and are separated by) normal brain parenchyma
Developmental venous anomaly (DVA
194
Imaging features of Developmental Venous Anomaly
“Medusa head” of dilated veins
Converge on large collector vein
195
\_\_\_\_\_\_\_\_\_\_\_\_\_\_is a collection of enlarged, thin-walled vessels resembling capillaries. The
vessels are surrounded and separated by normal brain parenchyma.
A brain capillary telangiectasia (BCT)
196
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_may cause vascular endothelial damage and induce development of multiple cavernous or
telangiectatic-like lesions in the brain parenchyma
Cranial irradiation
197
