Review
Pract Neurol: first published as 10.1136/practneurol-2020-002806 on 29 December 2020. Downloaded from http://pn.bmj.com/ on November 30, 2022 at University of Edinburgh. Protected
1
Department of Radiology,
St Vincent's Hospital Sydney,
Darlinghurst, New South Wales,
Australia
2
Department of Radiology,
Nepean Hospital, Penrith, New
South Wales, Australia
3
Department of Neurology,
St Vincent's Hospital Sydney,
Darlinghurst, New South Wales,
Australia
Correspondence to
Dr Joga Chaganti, Department
of Radiology, St Vincent's
Hospital Sydney, Darlinghurst,
New South Wales, Australia; ​
joga.​chaganti@​svha.​org.​au
Accepted 9 November 2020
Published Online First
29 December 2020
© Author(s) (or their
employer(s)) 2021. No
commercial re-­use. See rights
and permissions. Published
by BMJ.
To cite: Chaganti J,
Woodford H, Tomlinson S, et al.
Pract Neurol 2021;21:101–
107.
Black blood imaging of intracranial
vessel walls
Joga Chaganti,1,2 Hannah Woodford,2 Susan Tomlinson ‍
Sophie Dunkerton,3 Bruce Brew3
ABSTRACT
Traditional vascular imaging focuses on non-­
invasive cross-­sectional imaging to assess luminal
morphology; however, the vessel wall itself
may be specifically involved in many diseases.
Newer pulse sequences, and particularly
black blood MRI of intracranial vessels, have
brought a paradigm shift in understanding
the pathophysiology of many vasculopathies.
Black blood MRI of intracranial vessel walls
can help in a range of pathologies with
differing pathophysiology, including intracranial
atherosclerosis, aneurysms, vasculitis and
vasculopathy, moyamoya disease, dissection and
vertebrobasilar hypoplasia. This review highlights
how vessel wall imaging can contribute to the
clinical diagnosis and management of patients
with intracranial vascular pathology.
INTRODUCTION
Vascular imaging has traditionally meant
catheter angiography but more recently has
come to imply non-­invasive cross-­sectional
imaging, such as CT angiography and MR
angiography. However, catheter angiog-
raphy and cross-­ sectional angiographic
techniques can only assess the blood vessel
lumen. The vessel wall is involved in many
diseases and its structure is crucial for
understanding the underlying pathology.
The challenges in vessel wall imaging across
the body, and especially for intracranial
vessels, include artefacts associated with
flowing blood, dense bones that surround
them and the diameter of the vessel. Newer
pulse sequences have brought about a para-
digm shift in unravelling the underlying
pathophysiology of several vasculopathies,
thereby facilitating management. Here, we
discuss the clinical application of vessel wall
imaging techniques in the intracranial arte-
rial diseases with particular focus on black
blood (BB) MRI.
BACKGROUND
Intracranial vessel wall imaging is chal-
lenging. Impediments to imaging the
Chaganti J, et al. Pract Neurol 2021;21:101–107. doi:10.1136/practneurol-2020-002806
‍ ,3
vessel wall comprehensively include the
complex vessel wall course, the smaller
diameter of the vessels and flowing
blood with surrounding cerebrospinal
fluid (CSF) pulsations. Overcoming
these difficulties requires imaging with
adequate suppression of the signal from
blood flow as well as CSF together with
high-­resolution isotropic (a voxel that is
uniform in all directions).
BB MRI is a general term that describes
this type of pulse sequence, which
suppresses the signal from both the
flowing blood and CSF. Short-­axis plane
imaging (perpendicular to the long axis of
the vessel wall), obtained either directly
or by reconstructions from thin section
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isotropic imaging data, is ideal for iden-
tifying focal thickening of the vessel wall.
The vessel wall characteristics studied
in this type of imaging are typically the
morphology of the wall thickening and
pattern of enhancement. The pattern
of distribution gives clues to the type of
pathological process and is best done with
administration of contrast.
The intracranial vessel wall has four
layers: tunica intima, internal elastic
lamina, tunica media and tunica adven-
titia. The external elastic lamina that sepa-
rates the tunica media and adventitia is
absent in the intracranial arteries from the
point of their dural penetration. Current
MR scanners, even at 3T, cannot differ-
entiate the individual layers of the intra-
cranial vessel wall. However, BB imaging
techniques can identify disturbances in
the diseased arterial wall, including intra-
mural and periadventitial changes.
Typical BB MRI techniques include T-1
and T-2-­based acquisitions to characterise
the vessel wall abnormalities, with T-1
techniques repeated post contrast to char-
acterise the morphology and pattern of
enhancement further. Initial studies used
long variable flip angles to suppress the
signal from flowing blood. However, the
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current sequences use motion sensitised perpetration
pulse sequences or delay alternating with nutation
for tailored excitation to achieve both CSF and blood
suppression.1 2 Some vendors have incorporated alter-
native methods, such as inversion recovery prepara-
tions with repetition time and inversion time chosen
to get the steady state magnetisation to zero. These
techniques can be used in two-­dimensional and three-­
dimensional (3-­ D) sequences; however, the signifi-
cantly tortuous vessels of the intracranial circulation
make 3-­D acquisition preferable to enable reconstruc-
tion of any given vessel in multiple planes.
Normal vessel wall morphology
Normal vessel wall morphology is best assessed in the
proximal vessels of the circle of Willis as the vessel
diameter is relatively larger. The reported sizes of the
major vessels at the level of circle of Willis are: internal
carotid artery: 4.2 mm (±0.43 SD), anterior cerebral
artery: 2.09–2.2 mm (mean 2.14) and middle cere-
bral artery—M1 branch: 2.8–2.9 mm (mean 2.85). A
normal arterial wall has uniform thickness and should
not enhance.
Enhancement of the intracranial arteries gener-
ates considerable discussion as visually characterised
enhancement is subjective and prone to error. To
address this, enhancement of the vessel wall compared
with the enhancement of the pituitary stalk (an arbi-
trary standardisation as the pituitary stalk does not
have the blood–brain barrier as well) has been taken
as the internal standard and characterised as absent
(grade 0), less than the pituitary stalk (grade 1) or equal
or greater than the pituitary stalk (grade 2: marked).
Vessel wall enhancement relates to vessel wall inflam-
mation or damage and increased vasa vasorum density
that is usually associated with different vascular
pathologies.3
INTRACRANIAL ATHEROSCLEROTIC DISEASE
Intracranial atherosclerosis causes up to 25% of the
identifiable causes of ischaemic stroke. Using vessel
wall imaging, some strokes initially thought to be
cryptogenic were subsequently characterised and
attributed to intracranial atherosclerotic disease.4
Indeed Schaafsma et al recently showed that vessel
wall imaging in ischaemic stroke or transient ischaemic
attack altered the aetiological stroke classification in
55% of patients, primarily due to increased detection
of intracranial atherosclerotic disease lesions.5
Stenotic versus non-stenotic intracranial atherosclerotic
disease
The severity of vessel wall stenosis has been considered
the main target for clinical treatment and research.
However, vessel wall inflammation and the nature of
the vessel wall pathology are significant risk factors for
plaque rupture leading to stroke.6 Vessel wall changes
relate to growth of the plaque leading to remodelling;
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Figure 1  Top row: negative remodelling. (A) Precontrast
black blood (BB)-­concentric thickening of the vessel wall with
luminal narrowing. (B) Post contrast showing enhancement
and severe luminal compromise. (C) Time of flight (TOF) study
showing marked mid basilar stenosis. Bottom row: positive
remodelling. (D) Precontrast BB showing eccentric thickening of
the wall with little luminal narrowing. (E) Post contrast showing
enhancement of the eccentric thickening of the plaque. (F)
Shaded surface display of TOF showing no appreciable lumen
deformity.
expansion into the vessel lumen leads to luminal
narrowing (negative remodelling) whereas expansion
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away from the lumen causes little luminal compromise
(positive remodelling). Conventional imaging tech-
niques can identify the narrowed vessel lumen (nega-
tive vessel wall modification) but cannot characterise
the plaque and positive remodelling (figure 1).7–9
Multiple studies outside the intracranial environment
have shown that inflammation and positive remodel-
ling can lead to plaque rupture with a very high risk of
distal embolisation.
Characterisation of the plaque
An unstable plaque has a high propensity to embolise
distally and therefore requires more intense-­targeted
therapy. Inflammation, intraplaque haemorrhage,
positive remodelling in addition to the composition of
the plaque (calcific vs non-­calcific) each contribute to
this instability and may be independent of the vessel
wall narrowing. Furthermore, showing the state of the
vessel wall beyond the stenosis is a very useful when
planning endovascular therapy. BB MRI can address
these issues.
Histologically, a typical atherosclerotic plaque
shows focal calcification, a lipid core and a fibrous
cap with varying degrees of dominantly macrophage-­
mediated inflammation and vascularisation, possibly
with haemorrhage.
On BB MRI, the plaque is usually eccentric and
the vessel wall irregularly thickened with variable
enhancement of the fibrous cap.9–11 The plaque has
a characteristic T-2 hyperintensity corresponding to
Chaganti J, et al. Pract Neurol 2021;21:101–107. doi:10.1136/practneurol-2020-002806

the fibrous cap (80% sensitivity).12 13 The fibrous cap
often enhances and is characteristically eccentric.9 10 In
contrast, the T2 hypointense component of the plaque
corresponds to areas rich in foamy macrophages and
proteoglycans, and the lipid rich necrotic core. These
changes may occur in the cervical carotid arteries and
are probably the same in the intracranial arteries,
though we need more data. The degree of T2 signal
hypointensity of the lipid core may vary with solu-
bility of the lipids, for example, a solid core is more T2
hypointense than a liquefied lipid core at least in the
cervical carotid arteries.14 Increasing size of the lipid
core increases the risk of plaque rupture.
Atheromatous plaques are typically eccentric
although occasional plaque may be circumferen-
tial mimicking reversible cerebral vasoconstriction
syndrome and vasculitis. However, neither of these
have the T-2 hypointense wall that distinguishes the
intracranial atherosclerotic disease from the other
vasculopathies.
Non-stenotic intracranial atherosclerotic disease
This condition can compromise cerebral tissue perfu-
sion. Subtle atherosclerotic changes in the relevant
vascular territories, including wall thickening with
positive remodelling, may develop in non-­ stenotic
arteries in patients with stroke when compared with
controls. Similarly, deep white matter hyperintensities
identified on routine clinical imaging strongly associate
with non-­stenotic intracranial atherosclerotic disease,
which on BB MRI shows atherosclerotic changes to be
the most significant risk factor for white matter hyper-
intensities.11 15
Symptomatic versus asymptomatic plaques
BB MRI can differentiate symptomatic plaques from
asymptomatic plaques. Plaque features detected by BB
MRI, such as enhancement and haemorrhage, relate
prospectively to subsequent strokes (figure 2).
The plaque enhancement is due either to inflamma-
tion or to neovascularisation, or both. Plaques with
stronger enhancement appear to have a greater risk
of stroke. Indeed, studies have shown that the stroke
risk appears higher in patients with vessel wall reduc-
tion of 50% due to an enhancing plaque as opposed
Figure 2  Axial black blood vessel wall imaging showing
enhancing eccentric plaque (blue arrows) in the right posterior
cerebral artery territory and left supracavernous internal carotid
artery in a patient with multiple recurrent transient ischaemic
attacks with visual symptoms.
Chaganti J, et al. Pract Neurol 2021;21:101–107. doi:10.1136/practneurol-2020-002806
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to a similarly narrowed vessel due to a non-­enhancing
plaque. A recent study using 3T BB MRI on 138
patients with symptomatic atherosclerotic plaque of
varying degrees of stenosis found that of the 108 who
were followed for a median of 18 months, there were
39 strokes, of which 37 were in those with enhancing
plaques, giving an HR of 7.42 for recurrent stroke
among the patients with enhancing plaques.16 Case
reports with similar results have reinforced these data,
suggesting that plaque enhancement is a strong inde-
pendent variable for stroke risk. Furthermore, there is
some evidence that vessel wall enhancement after clot
retrieval is associated with poor clinical outcome and
increased infarcted volume, though the mechanism is
not clear.17
Intraplaque haemorrhage increases the risk of
stroke, at least in extracranial disease. BB MRI-­defined
intraplaque haemorrhage within the carotid plaques
strongly correlates with the histological findings.17
However, there are few studies on intraplaque haemor-
rhage with regard to the intracranial vessels due to the
diameter of small arteries and difficulty in obtaining
postoperative or postmortem correlation. Newer
sequences such as magnetisation-­ prepared gradient-­
echo (GRE) can assess intraplaque haemorrhage with
a high degree of sensitivity. Yu et al used this sequence
in patients with basilar artery stenosis, and showed an
80.9% accuracy of predicting the symptomatic plaque
by copyright.
(plaque with haemorrhage).6 18
In a recent meta-­analysis of studies of BB MRI in
intracranial atherosclerosis (20 studies), Lee et al
concluded that there are three imaging markers for
unstable intracranial plaques: contrast enhancement,
positive remodelling and plaque irregularity. Early
management seems to lead to better clinical outcomes,
emphasising the importance of early detection.12
BB MRI appears more sensitive than time of flight
(TOF) MR angiography in detecting luminal stenosis.
A recent study of 17 patients (with a total of 286 vessel
segments) found BB MRI had high sensitivity (92.5%)
and specificity (82.1%) for luminal stenosis assess-
ment using 3-­D -­TOF as a reference standard, while
3-­D -­TOF had only low sensitivity (59.4%) for plaque
detection.19
ANEURYSMS
Unruptured aneurysms are found in 3%–5% of popu-
lation. Even though most do not rupture, those that
do are associated with high morbidity and significant
mortality. Therefore, it is crucial to identify at-­
risk
aneurysms early. Several studies have suggested that
aneurysmal wall enhancement on BB MRI might help
to identify those unruptured aneurysms at higher risk
of rupture.20
Using BB MRI techniques aneurysms have been
studied for their morphology, risk of future leak/
bleeding and in the detection of the culprit aneurysm
in patients with subarachnoid haemorrhage associated
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with multiple aneurysms. Vessel wall enhancement
is strongly associated with aneurysm instability and
likelihood of rupture even when aneurysms are of
the same size. Conversely, the lack of wall enhance-
ment strongly predicts aneurysm stability.20A recent
meta-­analysis showed that BB MRI has a sensitivity of
95.0%, specificity of 62.7%, positive predictive value
of 55.8% and negative predictive value of 96.2% in
identifying unstable aneurysms. BB MRI in patients
with idiopathic subarachnoid haemorrhage may also
identify the vascular abnormalities missed with other
techniques including angiography.
Ruptured versus unruptured aneurysms
Although there are no available large data sets of
aneurysms assessed by BB MRI, multiple reports
have suggested that the technique is likely to identify
the culprit aneurysm in patients with subarachnoid
haemorrhage and multiple aneurysms.21 A thickened
enhancing vessel wall leading into an aneurysm is
thought to be very suggestive. Nagahata et al studied
117 patients and identified vessel wall enhancement in
up to 73% of ruptured aneurysms compared with less
than 5% of unruptured aneurysms. One further study
of 11 patients with subarachnoid haemorrhage and
normal digital subtraction angiogram identified arte-
rial enhancement near the likely sites of aneurysmal
rupture/thrombosis.13
These BB MRI defined features, namely thick-
ened wall with enhancement, have been verified by
histopathological studies, showing increased cellu-
larity, neovascularisation and diseased vasa vasorum.
Circumferential enhancement of the vessel wall
appears to be more sensitive for the risk of aneurysmal
rupture compared with size, depth and presence of
thrombus.22
After endovascular treatment, BB MRI of the aneu-
rysm wall may give information about the risk of
vasospasm. Early investigations found that persistent
enhancement in these vessel walls after therapy is
significantly associated with angiographic vaso-
spasm.10 23 In a more recent study, Moss-­Basha et al
observed that the second-­order and third-­order vessel
enhancement of the intracranial carotid branches after
coiling was significantly associated with angiographic
Figure 3  Aneurysm from the posterior inferior cerebellar artery with wall enhancement. (A) Black blood unenhanced study
showing posterior inferior cerebellar artery aneurysm, (B) T-2 axial study, (C) eccentric enhancement of the wall of the aneurysm and
(D) magnetic resonance angiography (MRA) showing no luminal abnormality.
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vasospasm, even after controlling for modified Fisher
grade (figure 3).24
VASCULITIS AND VASCULOPATHY
Vasculopathy is a general term used to describe any
disease affecting blood vessels. The spectrum of vascu-
lopathies includes vascular abnormalities caused by
degenerative, metabolic and inflammatory conditions,
and vasospastic disorders such as posterior reversible
encephalopathy syndrome. Vasculitis, on the other
hand, is a more specific term and is defined as inflam-
mation of the wall of a blood vessel.
Intracranial vasculitic disorders are subgrouped
according to the size of the involved vessels into
large, medium and small vessel. The pathogenesis is
presumed to be immune-­mediated inflammation of the
arterial wall. The diagnosis is often difficult and cere-
bral angiography is the current technique of choice.
The diagnostic hallmark on catheter angiography is a
beaded appearance of the intracranial arteries, which
may also have variable degrees of stenosis, occlusion
and rarely aneurysm formation. However, none of
these findings is consistent; indeed, they have a very
low sensitivity.
Given the general sensitivity of BB MRI, many inves-
tigators have used it to identify the changes associated
with vasculitis. These are (1) circumferential wall
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thickening, (2) circumferential grade 2 enhancement,
(3) smooth and concentric wall enhancement and (4)
iso/hypointense wall on T-2 similar to grey matter (in
contrast to atherosclerosis, which has high T2 inten-
sity in the walls).25
The vessel wall thickening and enhancement in
vasculitis are said to be more generalised, more uniform
and of greater intensity compared with atheromatous
enhancement. Previous studies have suggested that the
intensity of enhancement may differentiate vasculitis
from intracranial atherosclerotic disease (figure 4).10
The presence of periarterial/periadventitial enhance-
ment is characteristic, particularly in active disease,
though not all cases have smooth circumferential
enhancement and rarely the vessel wall may appear to
be normal (figure 5).11 Treatment variably improves
vessel wall enhancement, but the reasons are unclear.25
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Figure 4  Top row A and B (patient with known scleroderma
presenting with stroke): cortical infarct in the left posterior
parietal lobe with some haemorrhage and post contrast
black blood imaging showing vessel wall enhancement more
diffusely. (C) Post treatment with immunosuppressive drugs
and corticosteroid showing remarkable reduction in contrast
enhancement. (D, E) A patient known to be antineutrophil
cytoplasmic antibody positive but yet unclassified vasculitis
showing diffuse enhancement of the branches of middle
cerebral arteries.
26
Vessel wall enhancement is attributed to the increased
endothelial permeability with contrast leakage from
the lumen into the arterial wall. Vasa vasorum-­related
contrast leakage is a potential alternative mechanism
of wall enhancement.21
BB MRI may also help in making a definitive patho-
logical diagnosis. In a series of nine patients with
vasculitis, Zieler et al successfully identified a periph-
erally located inflamed vessel as a target for biopsy,
thereby reducing the known high false positivity with
biopsy (figure 6).27
Reversible cerebral vasoconstriction syndrome is a
non-­inflammatory vasospastic disorder, considered to
Figure 5  A suspected case of fibromuscular dysplasia/Takayasu arteritis showing (A) intense enhancement of the vessel wall of
right internal carotid artery (petrous segment), (B) digital subtraction angiogram showing gradual tapering of the right internal
carotid artery, (C) intense circumferential enhancement of the basilar artery and (D) however, luminal study (MR angiography time of
flight) does not show any evidence of luminal irregularity.
Chaganti J, et al. Pract Neurol 2021;21:101–107. doi:10.1136/practneurol-2020-002806
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Figure 6  Amyloid angiitis: (A) susceptibility weighted imaging
(SWI) show extensive siderosis. (B) Black blood vessel imaging
shows enhancing pial branches of the right middle cerebral
artery.
be part of the spectrum of vascular disorders associ-
ated with vascular permeability dysfunction. Vasculitis
is the principal differential diagnosis. Differentiation is
important, as the management is significantly different
despite common angiographic features. Reversible
cerebral vasoconstriction syndrome is treated with
observation or calcium channel blockers, whereas
vasculitis is treated with corticosteroids and immu-
nosuppressive drugs. Both conditions have multifocal
short segments of narrowing in different arterial terri-
tories resulting in a typical beaded appearance on
angiography. BB MRI can help differentiate the two
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by showing no or very little enhancement of the vessel
wall in reversible cerebral vasoconstriction syndrome,
although 5 of 48 patients in a recent study did had
marked enhancement that persisted for 7 months.28
Vasculopathy secondary to acute HIV infection and
illicit drug (cocaine) abuse can also cause vasospasm
with angiographic features mimicking reversible cere-
bral vasoconstriction syndrome. In cocaine abuse, the
vasospasm is a result of vessel wall inflammation. In
HIV, the pathogenesis is more complex and secondary
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to multiple factors leading to vessel wall inflammation
with progressive vasoocclusive morphology, vessel
wall thickening and enhancement in the acute phase.
MOYAMOYA DISEASE
Moyamoya disease is an uncommon cerebrovascular
disease characterised by progressive narrowing of the
supraclinoid internal carotid arteries with secondary
hypertrophy of the small collateral network, giving the
appearance of moyamoya (puff of smoke). It is more
common in people from east Asia. There is a bimodal
age distribution, at ages 5 and 40 years.29 Patholog-
ically, moyamoya disease is characterised by intimal
thickening in the walls of the terminal portions of
the internal carotid vessels bilaterally. This is associ-
ated with fibrocellular thickening of the intima, thick-
ening of the internal elastic lamina and thinning of the
media. Although the pathological involvement is bilat-
eral, the clinical presentation may not be. Moyamoya
disease develops in several conditions associated with
occlusion of the proximal internal carotid arteries
such as various connective tissue disorders, atheroscle-
rosis, phakomatoses (eg, neurofibromatosis type 1),
infections and previous radiotherapy. In older people,
moyamoya disease and intracranial atherosclerotic
disease can have similar morphology on angiography.
With BB MRI, moyamoya disease has concentric
enhancement of the distal internal carotid artery. In the
first large cohort study, Ryoo et al compared moyamoya
disease (32 patients) with intracranial atherosclerotic
disease (16 patients).30 Moyamoya disease showed
concentric enhancement of distal internal carotid
arteries and middle cerebral arteries (possibly repre-
senting hyperproliferation of wall components and
diffuse wall thinning with media shrinkage) regardless
of symptoms or stages, whereas patients with intra-
cranial atherosclerotic disease showed focal eccentric
enhancement in the symptomatic segment. Addition-
ally, the vessel wall in moyamoya disease characteristi-
cally shows shrinkage.29 30
DISSECTION
Intracranial arterial dissection is relatively rare. Diag-
nosis in small intracranial arteries is challenging though
the findings are still those of an intramural haematoma
and intimal flap, as with arterial dissection in other
vessels. Occasionally, there may be additional findings
related to the underlying cause such as vasculitis.31 32
Using a 3-­ D BB MRI technique, Mizutani et al
detected intramural haematoma in 87.5% of intracra-
nial arterial dissections with catheter angiography as
the gold standard.31 As elsewhere in the intracranial
system, 3-­D BB MRI is the technique of choice over
2-­D BB MRI. However, if 2-­D alone is used to image
the intracranial arteries, the reported sensitivity is
45%–65%.33 34
The eccentric vessel wall contrast enhancement iden-
tified in intracranial arterial dissection probably relates
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to inflammation, neovascularisation or decreased
blood flow within the false lumen.11 14 35 In addition,
the intimal flap dividing the true and false lumens may
show a high T2 signal.21
VERTEBROBASILAR HYPOPLASIA
Intracranial vertebral hypoplasia (defined as a luminal
diameter less than 2–3 mm) is not uncommon and can
be challenging to diagnose in the context of posterior
circulation territory ischaemia.36 It should be distin-
guished from other causes of luminal narrowing, such
as previous asymptomatic dissection with secondary
vessel wall remodelling, or atherosclerotic disease.
Luminal imaging cannot distinguish these three enti-
ties, whereas BB MRI shows a smooth vessel wall
usually with normal wall thickness and lack of vessel
wall enhancement.36
CONCLUSION
BB imaging techniques have extended our ability to
image the intracranial vasculature. Used together
with luminal imaging techniques, the technique has
furthered our understanding of the anatomical and
pathophysiological aspects of different vascular pathol-
ogies, facilitating clinical diagnosis and management.
by copyright.
Key points
►► Intracranial vessel wall imaging provides clinically
significant information on the vascular pathologies
and their underlying pathophysiology.
►► The technique has proven helpful in patients with
intracranial atherosclerosis, aneurysms, vasculitis
and vasculopathy, moyamoya disease, dissection and
vertebrobasilar hypoplasia.
►► The information on the vessel morphology and
enhancement patterns can characterise plaques in
atherosclerotic disease, identify high-­risk aneurysms
and improve detection of arterial dissection.
Further reading
►► Mandell DM, Mossa-­Basha M, Qiao Y, et al.
Intracranial vessel wall MRI: principles and expert
consensus recommendations of the American Society
of Neuroradiology. Am J Neuroradiol 2017;38:218–29.
►► Wang X, Zhu C, Leng Y, et al. Intracranial aneurysm
wall enhancement associated with aneurysm rupture:
a systematic review and meta-­analysis. Acad Radiol
2019;26:664–73.
►► Schaafsma JD, Rawal S, Coutinho JM, et al. Diagnostic
impact of intracranial vessel wall MRI in 205 patients
with ischemic stroke or TIA. Am J Neuroradiol
2019;40:1701–6.
Chaganti J, et al. Pract Neurol 2021;21:101–107. doi:10.1136/practneurol-2020-002806

Correction notice  This article has been corrected since it was
published Online First. Affiliations for HW and ST were
interchanged and have been amended accordingly.
Contributors  JC and BB conceived and wrote the review.
JC, BB and HW prepared the document. ST reviewed the
document and offered input on the included topics. ST
contributed to the literature review.
Funding  The authors have not declared a specific grant for this
research from any funding agency in the public, commercial or
not-­for-­profit sectors.
Competing interests  None declared.
Patient consent for publication  Not required.
Provenance and peer review  Not commissioned; externally
peer reviewed by Josh Klein, Boston, USA.
ORCID iD
Susan Tomlinson http://​orcid.​org/​0000-​0001-​9111-​0069
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