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Venous Ischemia 75
Fig. A4.23 Schematic drawing of the venous territories of the brain.
(Adapted from Schünke et al. [2006].) See p. XV for abbreviations.
size of the ischemic penumbra which, as shown in animal
experiments, seems to be larger in CVT (Frerichs et al.
1994). In patients with CVT, the area with a prolonged
mean transit time (MTT) in perfusion-weighted MRI can
be considered as the morphologic correlate of the penumbra (Doege et al. 2001). The large proportion of brain tissue
in CVT that is only functionally impaired explains the
frequently observed excellent clinical recovery even in
cases with delayed diagnosis and when venous congestion
infarcts or hemorrhage are present.
Similar to the arterial vascular territories, the venous
circulation also comprises areas that correspond to the
drainage of particular veins or sinuses (Fig.A4.23). The
dorsal frontoparietal regions of the cerebral convexity are
drained by ascending superficial veins, usually 12 on each
side which drain into the superior sagittal sinus. Each vein
drains a wedge-shaped area of the frontoparietal cortex.
One of these is the slightly dominating vein of Trolard
located over the postcentral region. Within the descending
veins, the vein of Labbé dominates the posterior aspects,
draining the blood from the lateral, basal and posterior
temporal lobe and itself draining into the distal end of
thetransversesinus,justatthejunctiontothesigmoid
sinus. The anterior regions, especially the areas around the
sylvian fissure are drained by sylvian veins which then run
toward the sphenoparietal sinus and the cavernous sinus.
The deepvenous system,comprising the paired basal veins
of Rosenthal and internal cerebral veins as well as the
straight sinus drains the temporomesial regions, large
aspects of the basal ganglia and the thalamus. Depending
on the affected vessels, a venous thrombosis may lead to a
corresponding venous territorial infarction as well as to
concomitant clinical symptoms (Fig. A4.24).
Symptoms are related to the location of thrombosis and
involvement of the parenchyma. In thrombosis of the
superior sagittal sinus without involvement of the adja-
Fig. A4.24 Top: Schematic drawing of venous infarct patterns.
(Adapted from Schünke et al. [2006].) Bottom: Corresponding radiologic examples. A,B Cortical/subcortical frontal lobe infarction in
ascending vein thrombosis. C, D Cortical/subcortical temporal lobe
infarction in vein of Labbé thrombosis. E, F Bilateral thalamic infarction and basal ganglia infarction in deep cerebral vein thrombosis.
cent cortical veins, patients may present with isolated
intracranial hypertension. The only clinical manifestations
may then be headaches and bilateral papilledema but no
focal neurologic signs. Sometimes an additional horizontal
diplopia may occur, caused by VI cranial nerve palsy. Extension of thrombosis to the ascending frontoparietal cortical veins will lead to circumscribed wedge-shaped infarctions which may resemble circumscribed arterial cortical
infarction. Focal motor or sensory deficits may be present
and are often associated with focal seizures with secondary generalization.The risk of seizures is particularlyhigh
if the Rolandic vein within the central sulcus or the vein of
Trolard in the postcentral sulcus is affected. Depending of
the site of a cortical vein thrombosis a variety of cortical
signs and neuropsychologic syndromes may occur. Because of the predominant distal affliction, the leg tends
to be more affected, and bilateral signs may be observed. In
transverse sinus occlusion, local signs such as otalgia and
cervical tenderness may be present. Venous infarction
within the temporal lobe may lead to aphasia or other
neuropsychologic deficits including confusion if the vein
of Labbé is affected. Venous temporal lobe infarction may
resemble partial territorial MCA infarction or herpes encephalitis. In cavernous sinus thrombosis, local signs are in
the foreground including orbital pain, chemosis, exophthalmus, and III—VI cranial nerve palsies. Thrombosis of
the deep venous system mainly lead to uni- or bilateral
infarctions of the basal ganglia and/or the thalamus. Bilateral thalamic infarction may also be caused by arterial
stroke if both thalamoperforating arteries are affected,
but the resulting infarct area is usually smaller in size
and spares the dorsal thalamic region. Clinically, not only
alterations of mood and consciousness but also extrapyramidal signs have been observed.
For neuroimaging and neurosonology in CVT, see also
Case 29 (p. 331).
76
5
Vascular Pathology
Vessel Wall Pathology .......................... 76
Elongations .................................... 76
Intima-mediaThickness.......................... 77
Atherosclerotic Plaques .......................... 78
Dissection ..................................... 80
Fibromuscular Dysplasia.......................... 80
Vasculitis ...................................... 81
Stenoses and Occlusions ........................ 81
Ultrasound Criteria of Stenoses ................... 81
Ultrasound Criteria of Occlusions.................. 85
Extracranial Pathology.......................... 86
ExtracranialAnterior Circulation................... 86
Vessel Wall Pathology
On investigation of the arteries supplying the brain, different types of vascular and vessel wall alteration may be
observed. These changes can be physiologic in nature or
may represent true pathologic findings.
Elongations
Vessel elongations are a frequent finding in extracranial
brain-supplying arteries (Fig. A5.1)andcanoftenbevisualized in proximal locations on duplex ultrasound
(Fig. A5.2). Their general reported incidence varies between 10% and > 40 %, depending on the studied population (Ballota et al. 2005, Huber 1982,La Barbera et al. 2006,
Perdue et al. 1975, Togay-Isikay et al. 2005, Weibel and
Fields 1965). Continuous strain due to long-term arterial
hypertension as well as vessel wall alterations within the
tunica media of the affected arteries have been previously
discussed as potential underlying precipitants (Del Corso
et al. 1998, La Barbera et al. 2006). Elongations can be
differentiated into three main groups (Fig. A5.3):
•C- or S-shaped elongation with angles > 90°.
• Coiling of the artery up to 360°.
• Kinking considered as a variant of coiling with an angle
<90°, actually prone to result in a lumen reduction and
subsequent vessel narrowing.
ExtracranialPosterior Circulation .................. 90
Intracranial Pathology .......................... 94
IntracranialAnteriorCirculation ................... 96
IntracranialPosterior Circulation................... 99
Collateral Pathways ............................ 101
IntracranialCollateral Pathways ................... 101
Intracranial Collateral Pathways in ICA Occlusive
Processes...................................... 105
Intracranial Collateral Pathways in VA Occlusive
Processes...................................... 108
ExtracranialCollateral Pathways................... 108
ClinicalRelevance ofCollateral Pathways ........... 109
Within the ICA, a straight vessel course is seen in 65–70 %
of individuals, a curved course in 23 %, and a coiled including kinking vessel in 9–16%. Following Weibel and Fields
(1965) an initial tortuous C- or S-shaped elongation over
about 4 cm in length occurs twice as often bilaterally than
unilaterally, affecting usually individuals older than 50
years. Coiling is usually found 4–8cmdistalofthebifurcation without side-to-side preferences and equal frequency
bilaterally and unilaterally without any reported age dependency. Routine ICA ultrasound insonation should
thereforebeperformedoverthewholevisiblevessel
length and as far distally as possible. Kinking involved
predominantly the ICA at 2 to 4cm distal of the bifurcation
and is more common in the elderly. Unilateral kinking is
twice as frequent as bilateral. There are no extensive analyses on the prevalence of kinking and the related grade of
stenosis. The clinical importance of these vessel changes is
currently debatable. Some authors regard elongations as
an anatomic variant without any clinical implications (Togay-Isikay et al. 2005), whereas others consider them
responsible for symptomatic cerebrovascular disease (Ballotta et al. 2005). Particularly problematic within this context is that coexistence of elongations and atherosclerotic
vessel changes is a frequent finding. Therefore a confident
differentiation of causal proportion is difficult. Whenever
elongations are found in symptomatic patients, careful
consideration should be given to whether the symptoms
match the affected vessel and if other potential causes are
not being overlooked.
Vessel Wall Pathology 77
Fig. A5.1 DSA, selective CCA filling, lateral view, of three patients
with distinct elongations (arrows) of the extracranial ICA in the A
distal segment, not accessible to ultrasound, B in the middle and
C proximal ICA, accessible to ultrasound (arrows).
Fig. A5.3 Left: Schematic drawing of the three types of vessel elon-
gation: A C- or S-shaped elongation with angles > 90°, B coiling of
the vessel up to 360°, C kinking with angles < 90°. Right: Corresponding color-mode images.
Fig. A5.2 Extracranial duplex, longitudinal view. Left: B-mode insonation. S-shaped ICA elongation. Right: Color-mode image of the
same vessel segment.
Fig. A5.4 Extracranial duplex, B-mode insonation, longitudinal
view. Left: normal IMT (0.5 mm). Right: Pathological finding with
raised IMT (1.4 mm).
Intima-media Thickness
Within the process of developing atherosclerosis the first
observable sign of vascular alteration may be an increasing
intima-media thickness (IMT). However, a raised IMT may
not only reflect atherosclerosis but also occur in other
conditions that lead to smooth muscle cell hyperplasia or
fibrocellular hypertrophy (Touboul et al. 2007). If extracranial insonation of the arterial vessel walls is performed
with insonation frequencies between 7 MHz and 15 MHz,
duplex ultrasound gives the best spatial resolution compared with any other imaging modality. According to the
Mannheim consensus criteria, IMT is defined as follows:
IMT is a double-line pattern visualized by B-mode sonography on both walls of the carotid arteries in a longitudinal image. It is formed by two parallel lines, which consist
of the leading edges of two anatomic boundaries: the
interface between the lumen and the intima and the interface between the media and adventitia (Fig. A5.4). IMT
measurements should be performed in regions without
atherosclerotic plaque, preferably the common carotid
artery (CCA), and may also be performed in the carotid
sinus as well as the internal carotid artery (ICA). If possible,
measurements should be made on the far wallas near-wall
evaluations are less reliable. For IMT determination either
an automated system or manual measurements can be
used. The former allows repeated measurements within
a predefined vessel segment (preferably 10 mm or longer)
in a short time, the latter requires rigorous quality control
to keep the intra- and interobserver variability low (Touboul et al. 2007). No consensus exists regarding the question of whether the maximum IMT or a mean IMT should
5 Vascular Pathology78
Tab l e A5 . 1 CCA IMT distribution in a population-based ultrasound analysis: Maximal wall thickness, combined data from the left and right
side. (From Howard et al. 1993.) Values above the 95th percentile can be considered as pathologic
Race Percentile Women Men
Age (years) Age (years)
455565 455565
White 25th 0.47 0.55 0.61 0.52 0.59 0.65
50th 0.54 0.62 0.71 0.60 0.68 0.77
75th 0.61 0.71 0.81 0.70 0.80 0.93
90th 0.68 0.82 0.94 0.80 0.91 1.11
95th 0.73 0.91 1.04 0.89 1.00 1.30
Black 25th 0.51 0.59 0.63 0.53 0.61 0.72
50th 0.58 0.68 0.74 0.62 0.72 0.85
75th 0.65 0.78 0.85 0.72 0.84 1.01
90th 0.73 0.91 1.00 0.83 0.96 1.22
95th 0.81 1.03 1.12 0.90 1.07 1.43
beusedandiftherightandtheleftsideshouldbeaveraged as IMT values seem to be higher on the left side
(Rodriguez Hernández et al. 2003). Population-based values of IMT vary depending on age, gender, and race (Table
A5.1) (Howard et al. 1993). Raised IMT values have been
associated with a number of classic vascular risk factors
such as hypertension, smoking, and cholesterol, and also
Fig. A5.5 Extracranial duplex, A–C B-mode insonation:
A longitudinal viewof the carotid bifurcation. Large near-wallplaque
(arrowhead) with pronounced acoustic shadowing (arrows).
B Cross-sectional view of the CCA: Semicircular, eccentric plaque
of largely homogenous medium echogenicity and a smooth plaque
surface (arrows). Note the circumscribed hypoechogenic lesion
within the plaque (middle arrow) which might be intraplaque hemorrhage or necrotic core. C Longitudinal view of the CCA: Multiple,
predominantly hyperechogenic plaques (arrows). D Color-mode insonation, longitudinal view of the carotid bifurcation, composed
image: Large hypoechogenic plaque (arrow).
with homocysteine levels, C-reactive protein, and the
presence of a metabolic syndrome or coronary artery disease (Crouse 2006). Prospective analyses have demonstrated that raised IMT values result in an increased number of myocardial infarctions and stroke in the elderly
population, indicating a predictive value for future vascular events (Lorenz et al. 2007, O’Leary et al. 1999).
Atherosclerotic Plaques
According to the Mannheim consensus criteria, atherosclerotic plaques are defined as follows: Plaque is a focal
structure encroaching into the arterial lumen of at least
0.5 mm or 50 % of the surrounding IMT value, or demonstratesathickness>1.5mmasmeasuredfromthemedia–adventitia interface to the intima–lumen interface
(Touboul et al. 2007). Atherosclerotic plaques can be further characterized by the following criteria (Figs A5.5 and
A5.6):
• Number: Singular, multiple.
• Location: Affected vessel, anterior/posterior wall, lateral
or medial wall.
• Form: Marginal, concentrical/circular, excentric/semicircular.
• Size:Lengthinlongitudinalsectionandthicknessin
cross section in mm.
• Echogenicity: Hyperechogenic, hypo-/anechogenic, homogenous or heterogenous pattern, calcification-induced acoustic shadowing.
• Surface: Regular smooth, irregular with recess/ulcerated.
• Vessel lumen reduction: Grade of stenosis.
Vessel Wall Pathology 79
Fig. A5.6 Extracranial duplex, longitudinal view of the carotid bifur-
cation. Left: B -mode insonation demonstrating homogenous mildly
hyperechogenic large plaque within the left carotid bifurcation. Note
the mild surface irregularity with a small plaque recess (arrow).
Right: Color-mode image of the same vessel segment demonstrating color filling of the recess (arrow).
Atherosclerotic vessel wall changes in the brain-supplying
arteries show a specific distribution pattern. According to
angiographic analyses in patients after cerebral ischemia,
stenoses are most frequently found at the extracranial
origin of the ICA followed by the origin of the vertebral
artery (VA), the subclavian artery (SA), and the intracranial
ICA, whereas vessel occlusions may be found at slightly
different preferential locations (Fig. A5.7).
Like IMT enlargement, the occurrence of carotid plaques
has been associated with several vascular risk factors.
Carotid plaque area has been shown to be a strong predictor of stroke, death, or myocardial infarction even after
adjustment for classic risk factors such as hypertension,
smoking, and cholesterol levels (Spence et al. 2006).
A large number of studies have tried to identify “highrisk” plaques by using the above morphologic ultrasound
criteria. Heterogenous echogenicity and ulcerated
plaques, i. e., with an irregular surface and/or recess,
have been postulated to be less stable and more likely to
cause embolic ischemic events. Also, hypoechogenic
plaquesseemtobemorelikelytobecomesymptomatic
than hyperechogenic plaques (el-Barghouti et al. 1996, Lal
et al. 2002, 2006, Park et al. 1998, Sabetai et al. 2000) (for
further details, see Case 1, p. 128). However, comparison of
ultrasound criteria and histopathologic findings in the
corresponding specimens, for example, from carotid endarterectomy show a moderate or poor correlation only
(Denzel et al. 2005). Histopathologic findings such as
fibrous cap configuration, necrotic core or intraplaque
hemorrhage are currently not satisfactorily accessible by
ultrasound methods and a large number of calcified
plaquesarenotatalldetectablebecauseofdistinctacoustic shadowing. Plaques in intracranial vessels cannot be
visualized by ultrasound. An unenhanced cranial computed tomographic (CCT) scan can be suggestive of rele-
Fig. A5.7 Distribution pattern of stenosis > 50% (A)andvesselocclusion (B),assessed by conventional angiography in patients following cerebral ischemia (adapted from Hass et al. 1968).
Fig. A5.8 Unenhanced CCT, axial plane. Left: Standard parenchymal
window setting, Right: Bone window setting. Top: Patient with distinct bilateral carotid siphon calcifications. Note the better delineation of plaque formation if the width of the window is changed to
bone window settings (arrows). Bottom: Patient with distinct VA
calcification, also delineated after change to a bone window setting
(arrow).
vant atherosclerosis as calcified plaques will delineate the
affected vessel segments, such as in the carotid siphon, the
VA,orthebasilarartery(BA)(Fig. A5.8). In case of an acute
vesselocclusionafreshemboluscanalsobedepictedby
CT. In case of a proximal M1-MCA occlusion a positive
middle cerebral artery (MCA) sign can be observed, and
in M2-MCA occlusion the so-called dot sign may be found
(Fig. A5.9). However, clear differentiation between the differential diagnosis of a thrombus/embolus or a calcification may be difficult in more peripheral vessel segments.
CT is particularly suitable for detecting calcifications of
the brain-supplying arteries but is less meaningful in the
analysis of plaque composition or surface description if
5 Vascular Pathology80
Fig. A5.9 Unenhanced CCT, axial plane, parenchymal contrast set-
tings. Left: Positive right-sided “media sign” resembling a fresh M1MCA thrombus which extends into the M2 segments (arrow). Right:
Right-sided positive “dot sign” (arrow) indicating cross-sectional
imaging of embolic M2-MCA branch occlusion.
Fig. A5.11 ICA dissection. A DSA, left CCA injection, lateral view:
Proximal occlusion of the ICA caused by a dissection. Note the typical
cone-shaped or “flame-like” occlusion (arrow). B, C Duplex ultrasound, longitudinal plane. B B-mode image demonstrating the
cone-shaped vessel narrowing (arrows). C Color-mode image demonstrates absent flow in the distal ICA (arrows).
Fig. A5.10 MRI, axial plane. A, B Enlarged T2-weighted image.
A Normal flow void in both A1-ACA and M1-MCA segments.
B MC A stenosis causing a reduced flow void within the right M1-
MCA segment (arrow). C Left: MRI, axial plane. Enlarged T2weighted image: Absent flow void within the left M1-MCA segment
in M1 occlusion (arrow). Right: Corresponding 3D TOF MRA with
absent M1-MCA signal (arrow).
detailed evaluation of the plaque surface. Non-contrast
sequences, in particular T2-weighted images, however,
permit the assessment of vessel patency by analysis of
the intravascular flow void (Fig.A5.10). If a CT scan or
MRI has been performed before the ultrasound examination, the available information about vessel wall pathology
should be taken into consideration.
Dissection
Ultrasound as well as digital subtraction angiography
(DSA),CTA,andMRIcanbeusedindiagnosisandfollowup of patients with dissections of the brain-supplying
arteries in the anterior and posterior circulations (Figs
A5.11, A5.12). However, in contrast to atherosclerotic vessel wall alterations, extracranial dissections are more distally located, which often limits their visualization by duplex sonography. For a more detailed discussion, see Cases
11 (p. 183) and 19 (p. 245).
Fibromuscular Dysplasia
compared to histopathologic findings (Denzel et al. 2005,
Oliver et al. 1999). In contrast, MRI is unable to depict
plaque calcification, but is able to visualize intraplaque
hemorrhage, necrotizing core, and fibrous plaque in vitro
and in vivo (Crouse 2006, Honda et al. 2007, Puppini et al.
2006). It may therefore be of particular value in the determination of high-risk plaques, especially in patients with
high-grade asymptomatic carotid stenosis (Crouse 2006,
Nighoghossian et al. 2005, Saam et al. 2006). Besides the
expensesof the method, the main currentMRI limitation is
its insufficient spatial resolution impairing especially a
The brain-supplying vessel segments most frequently affected by FMD (i. e., distal segments of the extracranial ICA
and VA) are not well accessible by duplex ultrasound. FMD
is therefore a diagnosis made by DSA, CTA, or contrastenhanced MRA. However, if proximal vessel segments are
affected, the irregular arterial vessel walls may also be
depicted by duplex ultrasound (Fig.A5.13). For a more
detailed discussion of FMD, see Case 13 (p. 204).
Stenoses and Occlusions 81
Fig. A5.12 Aortic archdissection DeBakey type I, extending into the
CCA. Duplex ultrasound. A Cross-sectional image of the CCA. Top:
B-mode image revealing a hyperechogenic membrane within the
vessel lumen. Bottom: Color-mode imagedemonstrates flowin both
lumina. B, C Longitudinal color-mode image and simultaneous
Doppler spectrum analysis of the CCA. B Sample volume within
the truelumen revealing areduced but unidirectional flow.C Sample
volume within the false lumen revealing a bidirectional flow pattern.
Vasculitis
Ultrasound, CTA, and MRI may be used in vasculitis of
large- and medium-sized arteries and DSA for all types
including small-vessel arteritis. Conditions accessible to
duplex ultrasound analysis are giant cell arteritis and Takayasu arteritis(Fig. A5.14).For a more detailed discussion
of giant cell arteritis, see Case 16 (p. 225), and for Takayasu
arteritis, see Case 23 (p. 279).
Stenoses and Occlusions
In general all segments of the extracranial and the relevant
parts of the intracranial brain-supplying arteries can be
assessed by duplex ultrasound, provided that the insonation conditions are good. The extent and order of ultrasound investigation should always be oriented according
to the clinical picture and other relevant clinical data such
as age, vascular risk factors, concomitant circumstances of
the cerebral ischemia, and suspected etiology, based on
radiologically documented stroke pattern if available before ultrasound examination. For instance, after cerebral
ischemia in the MCA territory, a proximal ICA stenosis or
occlusion is the most likely cause, which can be well accessed by duplex ultrasound. If no relevant pathology is
found, the distal extracranial ICA, the intracranial ICA in all
itsaccessiblesegments,aswellastheMCAinitsM1and
M2 segmentsmust be studied. In case of cerebellar orbrain
stem ischemia, the question of a V0-VA stenosis should be
the primary focus and if this is not found, a more distal VA
stenosis or occlusion or BA pathology has to be searched
for. In case of ischemia in the PCA territory, additional
Fig. A5.13 Fibromuscular dysplasia: Longitudinal color-mode image
and simultaneous Doppler spectrum analysis of the ICA. Irregular
color-filling of the artery with multiple areas of narrowing and raised
flow velocity of a maximum of 273/97 cm/s.
Fig. A5.14 Takayasu arteritis. Duplex ultrasound of the CCA.
A, B Cross-sectional plane. A B-mode image: Homogenous, mildly
hyperechogenic circular vessel wall thickening. B Color-mode im-
age: Color filling of the remaining arterial vessel lumen. C Colormode, longitudinal plane of the same vessel segment. D Longitudi-
nal color-mode image and simultaneous Doppler spectrum analysis
of the CCA with a raised flow velocity of 193/52 cm/s.
examination of the total visible PCA length has to be performed.
Ultrasound Criteria of Stenoses
Within the extracranial brain-supplying arteries, duplex
ultrasound permits the morphologic analysis of the affected vessel segment. Direct and indirect hemodynamic
effects of stenoses may be assessed in all extra- and intracranial brain-supplying arteries. For exact assessment of a
5 Vascular Pathology82
stenosis all accessible criteria should be considered. The
proximal extracranial ICA is not only the most commonly
affected site but can also be used to explain the main
ultrasound principles of vessel disorders. The following
remarks are mainly based on studies of the extracranial
ICA.
Direct Morphologic Assessment
Extracranial duplex ultrasound is able to visualize the
arterial vessel lumen near and at the carotid bifurcation,
the formation of intraluminal and vessel narrowing
plaques or even complete vessel filling, for example,
with thrombotic material. As the thrombotic material
canbehypoechogenic,analysisshouldalwaysbeperformed using the combination of B-mode and colormode ultrasound. The latter considerably facilitates the
detection of the residual perfused lumen and helps to
avoid overlooking, for example, a fresh, hypoechogenic
or small floating thrombus. Care should be taken to adjust
pulse repetition frequency and color gain to prevent color
overlapping beyond the perfused lumen. Limitations for
the direct morphologic ultrasound assessment may derive
from plaque calcification which may lead to pronounced
acoustic shadowing. This phenomenon might be observed
in up to 7 % of patients (Polak et al. 1989). Geometric lumen
reduction on B-mode and color-coded flow imaging can be
assessed in two ways: calculation of the reduction in the
cross-sectional diameter or the cross-sectional area.
Diameter
Diameter assessments can be performed in a longitudinal
plane, such as with DSA, but reliable measurements require a cross-sectional plane. Color-mode imaging facili-
tates the recognition of anechogenic material and is therefore recommended. Because of over-steering artifacts this
method is usually restricted to local stenoses < 50 %. Care
should be taken that the anterior and posterior walls are
simultaneously visible. Measurements are performed in
the region with maximal lumen reduction from the inner
border zone of the wall. The grade of stenosis is calculated
from the relation of the total vessel diameter (D
the minimal stenosis diameter (D
.
D
total
stenosis
)=D
stenosis
)and
total
× 10 0 %/
Area
In contrast with DSA, ultrasound also allows measurement
and calculation of the grade of stenosis from the crosssectional area, a parameter which correlates best with
results derived from postoperative histologic planimetric
analysis (Alexandrov et al. 1993, Eckstein et al. 2001). Area
measurement is also independent from the morphological
configurationof the stenosis,while the diameter approach
only measures correctly in the case of a circular shaped
stenosis. Therefore, the international consensus statement
recommends the measurement of area ratio for calculation
of stenosis (de Bray and Glatt 1995). The grade of stenosis
is calculated from the relation of the total vessel area
) and the minimal stenosis diameter (A
(A
total
A
stenosis
× 100 %/A
total
.
stenosis
)=
Examples of both diameter and area measurements are
given in Figure A5.15. Although assessed within exactly
the same vessel segment, both methods yield different
results. The diameter calculation (D
D
culation (A
= 3.4 mm) results in a 62 % stenosis, the area cal-
stenosis
= 52.4 mm2,D
total
=10.1 mm2)ina81%
stenosis
total
= 9mm,
stenosis. This phenomenon can also be described mathematically (Fig. A5.16). Depending on the type of stenosis
(axi-symmetric or asymmetric) the nonlinear relation between area and diameter varies in favor of diameter or area
(Spence and Reid 1979). As all major clinical trials so far
have used the diameter approach, it will currently continue to be the preferable assessment. In the future, however, the area method will gain importance, particularly
considering the rising use of CTA technique, with which it
is also possible to perform exact planimetric cross-sectional measurements (Bartlett et al. 2007).
Fig. A5.15 Extracranial duplex, cross-sectional view. A B-mode image: ICA filled with mildly hyperechogenic material, leading to an
excentric lumen narrowing. B Color-mode image: Confirmation of
the suspected stenosis. Note the color-overlap, slightly extending
beyond the remaining vessel lumen (arrow). C Diameter measurements: D
62 % stenosis. D Area measurements: A
circle), D
= 9 mm (green bar), D
total
=10.1mm2(red circle) resulting in a 81 % stenosis.
stenosis
= 3.4(red bar)resulting ina
stenosis
=52.4mm2(green
total
Direct Hemodynamic Assessment
Hemodynamic effects can be observed using the colormode of the ultrasound system. The color signal not only
reveals the regions with preserved flow but also gives
information about flow direction (orthograde or retrograde flow). Furthermore, a color aliasing phenomenon
may indicate the presence of raised flow velocities, such
as those caused by a stenosis. However, the main source of
hemodynamic information is provided by the Doppler
spectrum analysis from which several parameters can be
derived.
Blood Flow Velocity
Blood flow velocity values, i. e., the maximal systolic, maximal end-diastolic flow velocity or the mean flow velocity
are derived from the Doppler spectrum (for further details
see Chapter 3). Their assessment may reveal normal,
raised, or reduced values. Vessel narrowing is directly
correlated with raising flow velocities but this relation is
not linear over the whole range of stenosis grades. In very
high-grade stenosis and near occlusion, flow velocity
drops to normal or below normal values (Fig. A5.17).
If raised flow velocities are found, not only stenosis but
also other conditions haveto be considered.For example,a
global velocity increase may be observed in anemia, hemodilution or reactive hyperemia after head trauma or
general hypoxia. A local rise in flow velocities might be
seen in case of activated intracranial collateral pathways,
for example, in the anterior (ACoA) or posterior (PCoA)
communicating arteries or within vessel segments feeding
an arteriovenous malformation (AVM) or a dural fistula.
Generalized low flow velocities can be observed in severe
cardiac output failure or in the chronic state after severe
head trauma or hypoxia whereas regional blood flow reductions indicate hemodynamically relevant occlusive
processes proximal or distal to the measurement site.
Therefore, whenever flow velocities are assessed, the
underlying suspected disease as well as the time point of
insonation must be considered. For example, in case of a
severe global cerebral hypoxia the initial hours are characterized by a distinct reduction of cerebral blood flowand
subsequently the flow velocity. Subsequently a phase with
a reactive hyperemia can be observed, which comprises
generallyincreasedflowvelocitiesaswellasreducedpulsatilities. If the hypoxia leads to massive brain tissue necrosis, such as in persistent vegetative state, the chronic
phase may reveal low flow velocities and high pulsatilities
similar to the profiles seen in the external carotid artery
(ECA) (Fig. A5.18).
Stenoses and Occlusions 83
80
60
40
Area (% stenosis)
20
0
0 20406080
Diameter (% stenosis)
Fig. A5.16 Calculated relationship of stenosis grade using thediameter and area method. Blue line: Relation in axi-symmetric vessel
narrowing. A 30 % diameter stenosis equals about a 50 % areastenosis, a 70 % diameter stenosis equals about a 90 % area stenosis. Red
line: More linear relation between diameter and area stenosis in
severely asymmetric plaque formation and vessel narrowing.
Area reduction [%]
36 64 84 96
600
500
400
300
Blood flow (ml/s)
200
300
200
Flow velocity (cm/s)
CCA/ICA Index
The index is calculated from the maximal systolic flow
velocity within the ICA stenosis (V
ICA syst stenosis
)and
from the maximal systolic flow velocity within the nonaffected CCA (V
). It is a parameter that is independ-
CCA syst
ent from general blood flowalterations, but it only works if
the CCA can be assessed and it is itself not affected by
atherosclerotic vessel wall changes. CCA/ICA index = V
V
syst stenosis/
CCA syst
.
ICA
ICA/ICA Index
The index is calculated from the maximal systolic flow
velocity within the ICA stenosis (V
ICA syst stenosis
)and
from the maximal systolic flow velocity of the contralateral (nonaffected) ICA (V
ICA syst contralateral
). It only works if
the contralateral ICA shows normal flow profiles. Flow
velocity measurement should not be performed in the
carotid sinus but in a straight segment of the unaltered
100
0
020406080100
Diameter reduction [%]
Fig. A5.17 Mathematical flow model in ICA stenosis. Theoretical
relationship of stenosis grade (assessed by diameter and area measurements) and systolic blood flow velocity within the stenosis (blue
line). In ver y high-grade stenosis velocity values drop and further
decrease in near occlusion. Note the blood flow values remain constant until a 75–80 % diameter reduction (red line). (Adapted from
Spencer and Reid 1979.)
ICA. ICA/ICA index = V
ICA syst stenosis/VICA syst co ntralateral
100
0
Because of the referred limitation this index is not commonly used.
.
5 Vascular Pathology84
Fig. A5.18 Doppler spectra, obtained from follow-up transcranial
insonation of the MCA in a patient with severe hypoxia. A Normal
blood flow. B Hyperemia. Note the increased flow velocities as well
as the reduced pulsatility. C Reduced blood flow (hypoemia). Note
the reduced flow velocity as well as the increased pulsatility.
Fig. A5.19 Top: Schematic drawing of flow pattern ina normal and a
stenosed blood vessel. Bottom: Corresponding Doppler spectra.
Note the preserved systolic window in the unaffected vessel and
the turbulent flow with spectral broadening and increased velocity
within the stenosis.
Fig. A5.20 TCD Doppler spectrum of a high-grade stenosis (systolic
flow velocity > 300 cm/s). Note the mirror-image parallel strings as
the visual correlate of a musical murmur.
Flow Profile Alterations—Spectral Broadening
Doppler spectrum analysis of normal blood flowclassically
reveals a laminar flow characterized by a systolic window,
which means that its highest velocity is in the center of the
vessel and the lowest at its wall. In case of medium- to
high-grade stenosis the laminar flow changes to turbulent—in that only few erythrocytes flow very fast, the
majority are slow and nonlinear, resulting in raised Doppler spectrum intensities near the zero line (Fig. A5.19). In
very high-grade stenosis a harmonic phenomenon, the socalled musical murmur, can be observed. Acoustically it
resembles a bird cry and is therefore also frequently called
the “sea gull cry” or “goose cry.” In the Doppler spectrum,
mirror-image parallel strings or bands can be observed
(see Fig. A5.20 and video). The phenomenon presumably
results from harmonic frequencies, generatedfrom regular
vibrations of the vessel walls caused by the increased
blood flow velocities. Musical murmurs may be found in
extra- and intracranial stenosis. A recent study that reported on 66 musical murmurs found 94 % of murmurs
occurred in intracranial and 6 % in extracranial vessels (Lin
et al. 2006). In 88 % of cases a severe, high-grade stenosis
was detected. In the remaining cases, the musical murmur
was found mainly in the communicating intracranial arteries. Hereby the musical murmur indicates a “functional
stenosis,” when blood flow is too high for the size of the
ACoA or PCoA. As a rule of thumb it can be postulated that
whenever a musical murmur is detected intracranially,
and even if the maximal flow velocities are not clearly
raised, a high-grade stenosis or proximal stenoocclusive
process has to be present.
Both of the above criteria, spectral broadening and musical murmurs, however, are additional and not exclusive
criteria for stenosis. They depend on the grade as well as
the configuration of the stenosis and are not mandatory.
Indirect Hemodynamic Assessment
In any case of a suspected or known stenosis not only the
intrastenotic flow profile but also the flow profiles from
vessel segments proximal and distal to a stenosis (prestenotic and poststenotic flow signal) have to be analyzed.
This allows distinguishing between stenoses with or without a relevant hemodynamic effect. Proximal or distal flow
alterations are only seen in hemodynamically relevant
stenoses (Fig. A5.21). Stenoses are hemodynamically relevant if they cause a reduced blood volume flow and poststenotic pressure drop. According to a mathematical
model calculation applied to the ICA by Spencer and Reid
(1979) this occurs if the diameter is decreased by more
than 80 % or the cross-sectional area is reduced by 90–95 %
(Fig. A5.17). Archie and Feldtman (1981) found similar
results, suggesting a beginning of relevant blood flow
reduction of 40 % from 75 % diameter stenosis or 94 %
area stenosis onward. The Spencer curve (Fig.A5.17)can
be considered as a guide to study hemodynamic consequences in stenoses. As it refers to a circumscribed and