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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
Current Algorithm at the Charité University Hospital 125
serve for assessment of collateral circulation by the circle
of Willis, ophthalmic artery, and/or leptomeningeal vessels.
Contrast-enhanced MRA is less sensitive for plaque
composition and has an inferior spatial resolution. Nevertheless ce MRA has also been emphasized as an accurate
and cost-effective technique in patients with presumptive
higher-grade ICA stenosis (Wardlaw et al. 2006b). Both
techniques might also be very useful for the preinterventional disclosure of anatomic variants that might compro-
mise the procedure or prolong catheterization of the clinically relevant vessels. Due to the abundance of information available on MSCTA, concerning its length and diameter, and the vascular co-pathology of stenotic segments,
or size, morphology, and location of intracranial aneurysms, the neurointerventional and/or neurosurgical procedure is significantly enhanced. Assessment of stent and
vessel patency at the site of intervention as well as of
implant material integrity are further indications for
non-invasive angiographic imaging studies (Fig. A6.12).
Fig. A6.12 Peri- and postinterventional cervicocranial vasculature
assessment. A At a follow-up study to ICA stent angioplasty, stent
patency is confirmed by CTA (curviplanar image reconstruction).
B Following surgery on the internal carotid artery because of a
carotid glomus tumor, the patient developed a left-sided hemiplegia. CTA depicted right ICA occlusion and proximal ECA stenosis
(arrow). C MSCTA at the level of the aortic arch, volume-rendered
3D reconstruction, anterior oblique view. A stent disintegration is
shown (arrow). D MSCTA, volume-rendered 3D view of the lateral
skull. STeA-MCA bypass surgery, follow-up study showing good
patency of the bypass.
Part B: Case Histories
Degree of Neurosonologic Difficulty: Low
Case 1 Extracranial Internal Carotid Artery
Stenosis ............................. 128
Case 2 Free-floating Thrombus of the
ExtracranialInternal Carotid Artery ...... 133
Case 3 CommonCarotid Artery Occlusion ...... 138
Case 4 Temporal Arteriovenous Malformation . . . 143
Case 5 M1MiddleCerebralArtery Stenosis ..... 149
Case 6 P2Posterior Cerebral ArteryStenosis .... 156
Case 7 Cerebral CirculatoryArrest ............. 160
Case 8 Bilateral Intracranial V4 Vertebral
ArteryStenosis ....................... 165
Case 9 Moyamoya Disease with Bilateral
Carotid-T Stenosis..................... 171
Case 10 Thrombolysis of M1 Middle Cerebral
ArteryOcclusion...................... 176
Degree of Neurosonologic Difficulty: Medium
Case 11 Secondary Occlusion in Internal
CarotidArtery Dissection .............. 183
Case 12 Bilateral Proximal Extracranial Internal
Carotid Artery Occlusion and
High-grade V1 Vertebral Artery Stenosis . 194
Case 13 Internal Carotid Artery Stenosis in
Fibromuscular Dysplasia and Wegener
Granulomatosis....................... 204
Case 14 IsolatedCarotid SiphonStenosis ........ 210
Case 15 Near Occlusion of the Extracranial
InternalCarotid Artery................. 215
Case 16 Giant-cell Arteritis with Bilateral
Intracranial V4 Vertebral Artery Stenosis . 225
Case 17 Ascending Middle Cerebral Artery
Occlusion............................ 231
Case 18 Bilateral Internal Carotid Artery
Dissection ........................... 238
Case 19 Vertebral Artery Dissection with
Distal Occlusion ...................... 245
Case 20 Internal Carotid Artery Dissection
withFastRecanalization................ 251
Degree of Neurosonologic Difficulty: High
Case 21 Mid-basilar Artery Occlusion............ 261
Case 22 M1 Middle Cerebral Artery Occlusion
with Prominent Early Temporal Branch . . . 269
Case 23 Takayasu Arteritis with Subclavian Artery
and Vertebral Artery Stenoses .......... 279
Case 24 Dissection of the Extracranial Internal
Carotid Artery and Contralateral
M1 MiddleCerebral Artery Stenosis ..... 287
Case 25 Progressive M1 Middle Cerebral Artery
Occlusion............................ 297
Case 26 Extracranial Vertebral Artery
Dissecting Aneurysm following Basilar
ArteryStenting....................... 306
Case 27 Diffuse Cerebral Angiomatosis.......... 312
Case 28 Subclavian Steal Phenomenon in
Subclavian Artery and Internal Carotid
ArteryOcclusion...................... 319
Case 29 Cerebral Venous Thrombosis ........... 331
Case 30 Multilocular Extra- and Intracranial
Stenoses andOcclusions............... 338
128
Case 1
Extracranial Internal Carotid Artery Stenosis
Clinical Presentation
A 60-year-old woman presented with three transient episodes of right-sided loss of vision, each lasting a few minutes, in the 2 days preceding her admission. There were
no further episodes of transient focal neurologic deficits.
She had no vascular risk factors and was not on antiplatelet therapy. On admission, neurologic examination
including visual field and visual acuity was normal.
Initial Neuroradiologic Findings
There were no signs of ischemia on the initial computed
tomography (CT) scan.
Suspected Diagnosis
Recurring right-sided amaurosis fugax.
Questions to Answer by Ultrasound Techniques
• Was there evidence of high-grade stenosis in the right
internal carotid artery (ICA)?
• If so, what was the grade of stenosis?
Initial Neurosonologic Findings
Extracranial Duplex Sonography
B-mode sonography revealed no structural abnormality.
The color-flow image of the right ICA demonstrated a
reductioninthelumendistaltothecarotidbifurcation
caused by nonechogenic material. Doppler spectrum analysis in this area revealed a stenotic flow signal (flow velocity: 288/116 cm/s). Cross-sectional insonation confirmed
the marked reduction of the vessel diameter. Distal of
the stenosis the ICA Doppler spectrum demonstrated a
mild delayed systolic rise compared with the left side
(flow velocity: 65/17 cm/s). Flow in the common carotid
artery (CCA) was regular (flow velocity: 75/34 cm/s). There
were no pathologic findings in the left ICA (Figs. B1.1–
B1.6).
Transcranial Duplex Sonography
All detectable intracranial vessels including the OAs revealed normal and symmetric flow signals.
Conclusion
Right ICA stenosis of 70–80 %, directly above the carotid
bifurcation. The nonechogenic character of the stenotic
material was thought to be caused by either a smoothsurfaced “soft plaque” or a fresh, nonorganized intravascular thrombus.
Conventional Angiography
Digital subtraction angiography (DSA) demonstrated segmental narrowing of the superior aspect of the ICA with an
ulcerated surface, directly above the bifurcation. The extension of the stenotic segment was approximately 3 cm
(Fig. B1.7). The degree of stenosis (local measurement)
was estimated to be 80 %. There were no pathologic findings in the distal ICA or the middle cerebral artery (MCA)
on the affected side.
Clinical Course
Considering the three recurring transient retinal ischemic
attacks and the ultrasound finding of a nonechogenic
plaque, suggestive of a recent thrombus, the patient was
initially treated with partial thromboplastin time (PTT)guided heparinization instead of the usual treatment with
antiplatelet drugs. A cardiac embolic source was considered unlikely after transesophageal echocardiography and
24-hour electrocardiogram (ECG) demonstrated normal
findings. Seven days after admission the patient underwent carotid endarterectomy (CEA). Intraoperatively, a
soft plaque was removed, and there was no evidence of a
fresh thrombus. The operation and postoperative clinical
course were uneventful. No further ischemic attacks occurred, and the patient was prescribed clopidogrel for
long-term secondary stroke prevention.
Clinical Course
129
Degree of Neurosonologic Difficulty: Low
Fig. B1.1 Extracranial duplex, longitudinal plane. Normal flow signal
in the right CCA (flow velocity: 75/34 cm/s).
Fig. B1.3 Extracranial duplex, longitudinal plane. Color imaging of
the same region as in Figure B1.2 demonstrates a marked segmental narrowing.
Fig. B1.2 Extracranial duplex, longitudinal plane. B-mode imaging
of the right-sided carotid bifurcation including the right ICA appears
to be normal.
Fig. B1.4 Extracranial duplex, transversal plane. Cross-sectional
imaging of the right ICA reveals the true diameter of the artery.
Fig. B1.5 Extracranial duplex, longitudinal plane. Right ICA with
intrastenotic flow signal (flow velocity 288/116 cm/s).
Fig. B1.6 Extracranial duplex, longitudinal plane. Distal segment of
the right ICA revealing a mild poststenotic flow pattern (flow velocity: 65/17 cm/s).
Case 1 Extracranial Internal Carotid Artery Stenosis
130
Degree of Neurosonologic Difficulty: Low
Fig. B1.7 DSA, rightCCA injection, posteroanterior view.Segmental
narrowing of the right proximal ICA (arrows).
Final Diagnosis
Symptomatic high-grade stenosis of the right ICA with a
lumen reduction of about 70 to 80 % caused by anechogenic plaque.
Discussion
Clinical Aspects
The therapeutic decision of how to treat atherosclerotic
ICA stenosis is a matter of ongoing debate, with issues that
are of both scientific and emotive nature. Treatment strategies should be based on current scientific evidence.
The risk of ischemic stroke increases proportionately
with the degree of carotid stenosis. Randomized trials
have demonstrated that patients with severe ICA stenosis
benefit from CEA. While there has been long-term controversy as to whether surgery and catheter angioplasty
are comparable in terms of outcome as well as procedureassociated complications, recently published results from
the SPACEstudy indicate an equivalent risk profile for both
procedures (SPACE Collaborative Group 2006), which was
however highter than in the NASCET and ECST trials. Catheter angioplasty is relatively less invasive and more cost
effective and, as a result, might become an alternative
treatment of choice in symptomatic high-grade carotid
artery stenosis. However, comparative long-term followup analyses, e. g., of re-stenosis rates, are not yet available.
The decision between surgical and medical treatment remains difficult.
The differing therapeutic options for patients with
symptomatic and asymptomatic carotid artery stenosis
were addressed in two important large, randomized clinical trials, the North American Symptomatic Carotid Endarterectomy Trial (Barnett et al. 1998, NASCET 1991) and
the European CarotidSurgery Trial (ECST1991,1998).These
trials compared CEA with medical treatment, and the results of both were similar if the different methods used to
measure the degree of stenosis were adjusted (Rothwell et
al. 2003a, Rothwell et al. 2003b) (for further reading see
also chapter 5 “Extracranial Anterior Circulation,” p. 86).
Patients with symptomatic carotid stenosis > 50 % (NASCET
criteria) or > 79 %(ECST criteria) derived substantial benefit
from CEA, persisting five years or more. The number
needed to treat for preventing one ipsilateral disabling
ischemic stroke or death over 2 to 6 years follow-up was
15 for the >70% (NASCET) or >80% (ECST)symptomatic
carotidstenosis,and21forthe50–69 % (NASCET) or
70–80 % (ECST) symptomatic carotid stenosis. Patients
with lesser degrees of stenosis did not benefit (Cina et al.
2000). These findings were only valid if CEAwas performed
within the first 6 months following stroke or transient
ischaemic attack (TIA) with the greatest benefit within
the first 2 weeks (Rothwell et al. 2004). After 2 years, the
risk of stroke in medically treated patients was similar to
the low levels in surgically treated patients, potentially
explained by spontaneous plaque stabilization or gradual
improvement of collateral function over time. Furthermore, patients who had a near occlusion of the ICA also
did not benefit from surgery as their risk of embolic stroke
under medical treatment alone was very low. Near occlusion was defined by a poststenotic angiographic carotid
narrowing with an ICA/CCA ratio < 0.42 (Rothwell and
Warlow2000). Therefore in clinical practice,the frequently
demanded exact differentiation between ICA near occlusion and occlusion, for example by invasive DSA, might not
be as important as the assessment of sufficient collateral
function (see also Chapter 5, “Collateral pathways,” p.101).
Controversy persists regarding the appropriate management of asymptomatic carotid stenosis. Its prevalence
ranges from 0.5 % in individuals < 60 years of age rising
to 10 % in those > 80 years (Prati et al. 1992, Ricci et al.
1991). The overall annual risk of stroke in these patients is
1–3 % (ECST 1998), i.e., far lower than in those with recent
stroke or TIA (10% within the first year). Any therapeutic
strategy therefore requires a very low interventional risk
for patients to statistically and more important clinically
benefit from the procedure. Two multicenter studies, the
CASANOVA Study (CASANOVA Study Group 1991) and the
VA-Asymptomatic Carotid Stenosis Study (Hobson et al.
1993) showed negative results in the above patient group.
However, the recently published results from the Asymptomatic Carotid Surgery Trial (ACST), which included 3120
patients, showed a modest but significant absolute risk
reductionof5.4%at5years(AsymptomaticCarotidSurgery Trial [ACST] Collaborative Group 2004), which corresponds with the projected absolute risk reduction of 5.9 %
at 5 years previously reported by the Asymptomatic Carotid Atherosclerosis Study (ACAS) investigators (Executive Committee for the Asymptomatic Carotid Atherosclerosis Study 1995). The reported benefit resulted in a number needed to treat 50 patients to prevent 1 strokewithin 3
Discussion
131
years in the ACAS trial. This number was only valid if the
interventional risk of stroke or death due to CEA was
approximately 3 %—which seems quite low. In particular,
subgroup analysis showed no significant benefit from CEA
for women in ACAS. Although ACST reported such a benefit, the absolute risk reduction of 4.1 % seen in women was
only half of the absolute risk reduction observed in men.
Obviously some asymptomatic patients with ICA stenosis
face a much higher stroke risk than others and further risk
stratification is necessary to identify these patients. It
seems that asymptomatic patients will benefit from CEA
only if the perioperative risk is very low.
The exact assessment of risk and benefit has also to be
applied to the increasingly used percutaneous carotid angioplasty and stenting. These interventions have the potential to evolve as a therapeutic alternative to CEA, particularly in patients who are at increased risk of complications with surgery. The rates of complications in early
studies were much higher than in those using open surgery. However, the recently published Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS investigators 2001), which compared endovascular treatment with conventional carotid surgery, found no difference between the two procedures in the number of strokes
or deaths but only because the CEA group had a 9.9%
complication rate which was more than 2 times higher
than in NASCET and ECST. Stenting reduced the number of
some of the complications such as local wound infection,
local bleeding and cranial nerve palsy.It also shortened the
length of hospital stay and lowered the short-term treatment costs. However, the study did not demonstrate that
the procedure reliably prevented stroke over time. Stenting does not remove atheromatous plaque and the rate of
re-stenosis, potentially resulting in an unacceptable rate of
long-term stroke recurrence, seems to be greater than
after carotid surgery. The SPACE study failed to prove noninferiority of carotid artery stenting compared with CEA in
1200 patients with symptomatic ICA stenosis. The 30-day
incidence of ipsilateral ischemic stroke or death was 6.84%
in the stenting group and 6.34 % in patients after CEA
(SPACE Collaborative Group 2006). The French EVA3S
study was stopped prematurely after inclusion of 527
patients with symptomatic ICA stenosis ≥ 60 % because of
an obvious inferiority of the stenting treatment. The 30dayincidenceofanystrokeordeathwas3.9%afterCEA
and 9.6 % after stenting. However, in this study the skill
requirements of the treating physicians were remarkably
different. Surgeons were allowed to participate if they had
performed at least 25 CEAs in the year preceding the study
onset, whereas interventionalphysicians could participate
if they had only performed a total number of 12 ICA or 35
supraaortic artery stenting procedures, including five in
the ICA (Mas et al. 2006). At present, several ongoing major
randomized, multicenter trials addressing the above questions (CREST in the USA, ICSS in Great Britain) Also, longterm results are awaited from the German and Austrian
SPACE study.
In the future, risk stratification beyond the degree of
stenosis and the question of a prior ischemic event might
guide the therapeutic decision. For example, patients with
recent cerebral ischemia are at higher stroke risk than
patients with only retinal events. Patients with an irregular carotid plaque are at higher risk than those with
smooth plaques (Rothwell and Warlow 1999). Intracranial
atherosclerotic disease is an independent risk factor for
subsequent stroke in medically treated patients with
symptomatic ICA stenosis, enhancing the value of CEA in
patients with moderate symptomatic extracranial ICA
stenosis (Kappelle et al. 1999). In asymptomatic highgrade carotid stenosis, women appear to have a higher
postoperative stroke risk than men. In addition, patients
aged over 75 years, patients with a history of congestive
heart failure, and patients undergoing prophylactic CEA or
stenting for asymptomatic stenosis in combination with
coronary surgery are at high risk (Goldstein et al.1998).
Future studies will have to show if prognostic modeling
may identify other groups of patients who could particularly benefit from CEA or stenting in symptomatic as well
as asymptomatic patients.
Angiologic and Anatomic Aspects
The detection and quantification of carotid stenosis is one
of the important main indications for diagnostic ultrasound as the degree of stenosis has been shown to strongly
correlate with stroke risk.
Careful application of the following criteria leads to a
reliable ultrasound-based carotid stenosis assessment, not
only matching the gold standard results but also providing
additional hemodynamic parameters which cannot be derived by any of the competing methods. Grading of carotid
stenosis by means of color-coded duplex sonography is
based on two principles:
• Low-grade stenoses (< 50 %) can be assessed by geomet-
ric vessel lumen analysis (measurement of area and
diameter in the cross-sectional and longitudinal image)
using the B- and color-mode of the ultrasound system.
• Analysis of high-grade stenosis is based on hemody-
namic parameters, derived from pre-, intra-, and post-
stenotic Doppler spectrum analysis (see also Chapter 5,
“Stenoses and Occlusions,” p. 81, and “Extracranial Path-
ology,” p. 86).
Area measurements in high-grade stenosis can be performed for orientation, but should not be used for exact
graduation as the color-mode within a stenosis often suffers aliasing or color oversteering effects which may lead
to an underestimation of the real lumen reduction. In our
case, the Doppler spectrum analysis showed the hemodynamic findings of a high-grade stenosis of 70 to 80 % (local
grade of stenosis), correlating well with the angiographic
evaluation.
B-mode and color-mode imaging of carotid stenosis
alone has its limitations too, as acoustic shadowing caused
Degree of Neurosonologic Difficulty: Low
Case 1 Extracranial Internal Carotid Artery Stenosis
132
by plaque calcification as well as inadequate visualization
of the vascular wall might occur. Large and concentric
calcified plaques may completely obscure flow in a vessel
over several centimeters, impeding the evaluation of a
stenosis. If normal flow signals are found in the vessel
segments before and behind the lesion a stenosis > 80 %
seems unlikely. In our case, the intrastenotic flow velocity
of 288/116 cm/s, the slightly poststenotic flow pattern distal of the stenosis, as well as the missing activation of
intracranial collateral pathways strongly argue in favor of
a local stenosis of 70 to 80 % (see also Chapter 5, “Extracranial Pathology,” p. 86).
Degree of Neurosonologic Difficulty: Low
The carotid bifurcation is particularly susceptible to the
development of atherosclerotic lesions. This is mainly
caused by the anatomic characteristic of a frequently
present vessel widening of the carotid sinus. This leads
to turbulent blood flow causing altered mural tensile
stress and changes in compliance, composition, and metabolismofthearterialvesselwall.Thetrueinitiating
event for early plaque induction is still not entirely clear,
however, the above findings indicate that particularly flow
associated mechanical factors might predispose to plaque
formation.
Duplex ultrasound allows an opportunity to not only
grade carotid stenoses but also analyze plaque morphology. High-resolution ultrasound enables description of
atherosclerotic plaque by examining its echogenicity (anechogenic to echogenic), texture (homogeneous to heterogeneous), surface contour (smooth to rough), surface
motion (uniformto discrepant), and progression or regression in echogenicity. Histologic investigations have shown
that soft lipid-rich plaques present a higher embolic risk
than hard calcium-containing plaques (Bock et al. 1993).
Furthermore, plaques with ulcerated surfaces are associated with a higher rate of cerebral infarction than those
with smooth surfaces (el-Barghouti et al. 1996). Unfortunately sonographic characterization of the plaque structure only vaguely correlates with the histologic findings,
questioning the value of an extensive morphologic description. Some authors report an increased risk of plaque
rupture in association with sonographic findings of irregular border, echolucency, heterogeneity, length of stenosis,
plaque thickness, longitudinal pulsatile plaque movements, or speed of plaque progression (Park et al. 1998).
However, one has to keep in mind that only about onethird of all plaques can be visualized correctly by the ultrasound technique.
In our case, the missing B-mode signal during the initial
investigation of the stenotic material was suggestive of an
anechogenic “soft plaque” with a smooth surface or a fresh
intraluminal thrombus. Intraoperatively, a “soft plaque”
was removed
Ultrasound has to compete with DSA, computed tomographic angiography (CTA), magnetic resonance angiography (MRA), and contrast-enhanced MRA. Many reports
and studies have already reported indices, parameters,
and grading methods, generally concluding that no current single method can precisely quantify the degree of
carotid stenosis. Despite these methodologic disputes,
some authors exclusively favor duplex sonography,
whereas others consider DSA as an absolute necessity
despite the reported 1 % interventional morbidity, which
is probably even higher in symptomatic vascular patients
(see also Case 24, “Discussion,” p. 294).
Up to now DSA remains the gold standard method as the
NASCET and ECST studies are based on it. However, even
the DSA technique has limitations leading to imprecise
grading of stenosis. The underlying reason is that carotid
stenoses are almost never circular in shape. A single conventional DSA projection therefore comprises the risk of
stenosis over- or underestimation as has been shown if
compared with the “true” degree of stenosis in surgically
removed specimens (Alexandrov et al. 1993) while ultrasound or CTA are less prone to this potential source of
artifact. New 3D-computed rotational DSA techniques
might help to overcome the illustrated problem, however
the other less or noninvasive techniques are progressing
and will probably replace DSA at least for the purpose of
simply answering the question of stenosis evaluation. A
recent metaanalysis comparing noninvasive imaging of
symptomatic carotid stenosis with conventional angiography underscores this prediction (Wardlaw et al. 2006).
The metaanalysis included results of 41 studies, comprising the evaluation of 2541 patients and 4876 arteries.
Stenoses assessed by the ECST grading system or by the
common carotid artery method (CC) were converted into
NASCET grades (conversion formula: NASCET = (ECST or
CC-40)/0.6). For stenoses between 70 % and 99 % the sensitivity/specificity values for ce MRA, MRA, CTA, and duplex ultrasound were 0.94/0.93, 0.88/0.84, 0.76/0.94, and
0.89/0.84, respectively. For 50–69 % stenoses the corresponding values were 0.77/0.97, 0.37/0.91, 0.67/0.79, and
0.36/0.91. The data demonstrates that high-grade stenoses
may be almost equally well detected by either of the above
methods, while all methods are less accurate in assessing
less severe stenoses. Future clinical stroke trials in patients
with high-grade stenoses or study set-ups requiring a
repeated follow-up investigation might therefore rather
makeuseoneofthenoninvasivediagnosticmethods
which will subsequently and stepwise further reduce the
importance of DSA.
The current question therefore remains: which of the
above techniques will be the future method of choice? In
our opinion, ultrasound use will increase and become the
first-line investigation in routine clinical practice and follow-up examination because of its widespread availability,
low costs, and minimal patient discomfort. Contrast-enhanced MRA might become the most relevant confirmatory technique. However, CTA, which like the duplex ultrasound technique allows measurement of the real carotid
sinus diameter and the residual intrastenotic vessel lumen,hasmadetremendousprogress(Bartlettetal.
2007). Future studies will show which of the presented
methods either alone or in combination will serve as the
future gold standard.
Case 2
Free-floating Thrombus of the Extracranial Internal Carotid Artery
133
Clinical Presentation
A 54-year-old woman was admitted to the emergency
room with right-sided weakness and aphasia that had
started 50 minutes prior to her presentation. She had a
history of non-Hodgkin lymphoma, diagnosed 4 years
previously. She stopped taking methotrexate 2 days prior
to this admission because of the following hematological
abnormalities: thrombocytosis (750/nl; normal range
150–400/nl), leukopenia (3.86/nl; normal range 4.5–
11.0/nl) and anemia (93g/L; normal range 120–157 g/L) .
She was also taking oral steroids on a long-term basis for
coexisting Sjögren syndrome. The neurologic examination
on admission revealed incomplete motor aphasia, a mild
right-sided hemiparesis, and a right facial paresis (National Institute of Stroke Scale [NIHSS] score 7).
Initial Neuroradiologic Findings
Admission cranial computed tomography (CCT) showed
no signs of acute cerebral ischemia. Cerebral magnetic
resonance imaging (MRI) the following day revealed multiple small cortical and subcortical ischemic lesions in the
left anterior cerebral artery (ACA) and middle cerebral
artery (MCA) territory. A contrast-enhanced magnetic resonance angiogram of the extracranial brain-supplying vessels was initially reported to show normal findings
(Figs.B2.1–B2.3).
Suspected Diagnosis
Multiple small, embolic cerebral infarctions in the left ACA
and MCA territory.
Question to Answer by Ultrasound Techniques
• To find or exclude an embolic source in the left common
carotid artery (CCA) or internal carotid artery (ICA).
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode imaging of the left ICA distal to the carotid bifurcation displayed a lumen reduction of 50 % caused by a
mild hyperechogenic floating structure (12.5 ×5 mm) that
was partially adherent to the lateral vessel wall. Doppler
spectra and blood flow velocities were regular even at the
densest aspect of stenosis. There were no pathologic findings in the right CCA and ICA (Figs. B2.4–B2.6).
Transcranial Duplex Sonography
All detectable intracranial vessels revealed normal and
symmetric flow signals. However, several microembolic
signals were recorded during insonation of the left MCA
(Fig. B2.7).
Conclusion
Partially floating, unstable, continuously microemboli
emitting thrombus in the left proximal ICA causing a lumen reduction of about 50 %.
Clinical Course
Because of our patient’s complex hematologic history, rtPAtreatment was contradicted according to current guidelines. Instead of intravenous partial thromboplastin time
(PTT)-guided heparin was given to her. The pattern of
multiple small infarctions in the left ACA and MCA territory was suggestive of an embolic etiology, caused by the
floating thrombus located in the left ICA. On reevaluation
of the MR angiograms, a circumscribed signal of reduced
intensity was observed in the left ICA directly above the
carotid bifurcation, in accordance with the initial duplex
results (Fig. B2.8). Carotid endarterectomy was considered
to be the best treatment. The patient had surgery on the
same day (Fig. B2.9). Postoperative follow-up was uneventful.
Case 2 Free-floating Thrombus of the Extracranial Internal Carotid Artery
134
The etiology of the intravascular thrombus was unclear,
but the underlying hematologic disease with severe
thrombocytosis was suggestive for a paraneoplastic coagulopathy (anticardiolipin antibody levels were not
raised). Blood culture and transesophageal echocardiography excluded an infectious cause. The intravenous heparin was replaced by low-dose subcutaneous heparinization after 10 days, which was continued until a therapeutic
decision regarding the lymphoma was made. The neurologic deficits improved markedly and the patient was discharged with a mild right-sided hemiparesis and amnesic
aphasia.
Degree of Neurosonologic Difficulty: Low
Neurosonologic Findings (Day 20)
Follow-up ultrasound examination 2 weeks after discharge demonstrated a normal left ICA (Fig. B2.10).
Final Diagnosis
Multiple embolic infarctions within the ACA and MCA
territory caused by a partially floating thrombus in the
proximal left ICA. The presumed etiology was a paraneoplastic coagulopathy.
Fig. B2.1 MR diffusion-weighted image, axial plane. Ischemic lesions in the basal ganglia and in the left-sided MCA territory.
Fig. B2.3 Extracranial contrast-enhanced MRA, coronal MIP. Normal
aspect in the conventional MIP projection.
Fig. B2.2 MR diffusion-weighted image, axial plane. Multiple ischemic cortical lesions within the lef t-sided ACA and MCA territory.
Fig. B2.4 Extracranial duplex, longitudinal plane. Normal flow signal
in the left CCA (flow velocity: 95/37 cm/s)
Discussion
135
Degree of Neurosonologic Difficulty: Low
Fig. B2.5 Extracranial duplex, longitudinal plane. Normal flow signal
in the left distal ICA (flow velocity: 81/39 cm/s).
Fig. B2.7 TCCS (transtemporal approach), left-sided insonation,
upper pontine plane. Normal flow signal in the left M1-MCA (flow
velocity: 92/29 cm/s). Note the microembolic signal within the Doppler spectrum (arrow).
Fig. B2.6 Extracranial duplex, longitudinal plane. B-mode sonography reveals a floating thrombus (12.5 × 5 mm) that is partially adherent to the lateral vessel wall in the right proximal ICA, directly above
the carotid bifurcation, reducing the lumen by approximately 50 %.
Fig. B2.8 Extracranial contrast-enhanced MRA, coronal MIP. In accordance with the ultrasound findings, a review of the angiograms
revealed a circumscribed area of reduced signal intensity in the left
ICA, directly above the carotid bifurcation (arrowhead).
Discussion
Clinical Aspects
We have described a patient with multiple embolic infarctions within the ACA and MCA territory caused by embolic
fragments from a free-floating thrombus within the left
ICA. The patient had a history of non-Hodgkin lymphoma
and developed severe thrombocytosis and anemia after
chemotherapy with methotrexate. Hypercoagulability is a
well-known paraneoplastic syndrome associated with
several hematologic malignancies. Clinical incidence of
thromboembolic disease in cancer patients ranges from
1 % to 11 % but has been reported in up to 50 % of cases at
autopsy (Frenkel and Bick 1998). Hypercoagulability is
thought to arise from interactions between tumor cells,
endothelial cells, macrophages, and platelets as well as
from procoagulatory and fibrinolytic factors associated
with the tumor cells themselves. The tumor cells may
produce specific tissue factors or cancer procoagulants,
both of which activate factor X (Falanga and Rickles 1999).