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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
Case 12 Bilateral Proximal Extracranial Internal Carotid Artery Occlusion and High-grade V1 Vertebral Artery Stenosis
196
Hemodynamics,” p. 60). Therefore, no interventional therapy (e. g., intracranial EC-IC bypass or stenting of the VA
Final Diagnosis
stenosis) was recommended and the patient was started
on clopidogrel for long-term secondary stroke prevention.
The clinical symptoms almost completely remitted over
the following weeks. Three-year follow-up revealed no
further clinical events, and the neurosonologic findings
were unchanged.
Degree of Neurosonologic Difficulty: Medium
Bilateral border zone infarctions and left embolic MCA
territorial infarction in bilateral extracranial ICA occlusion,
probably as a result of atherosclerosis. Good collateralization via the posterior circulation. High-grade asymptomatic proximal left VA stenosis.
Fig. B12.5 Extracranial duplex, longitudinalplane. Right CCA Doppler spectrum with increased pulsatility (flow velocity: 47/8 cm/s).
Fig. B12.7 Extracranial duplex, longitudinal plane. Right ICA with
occlusion 1cm above the carotid bifurcation.
Fig. B12.6 Extracranial duplex, longitudinal plane. Left ICA without
color signal due to anechogenic material, directly above the carotid
sinus (arrows).
Fig. B12.8 Extracranial duplex, longitudinal plane. Normal flow signal in the left external carotid artery (ECA) with typical oscillation
effect on mild manual oscillation of the temporal artery.
Final Diagnosis
197
Degree of Neurosonologic Difficulty: Medium
Fig. B12.9 Extracranial duplex, longitudinal plane. Normal flow sig-
nal in the right ECA with typical oscillation effect on mild manual
oscillation of the temporal artery.
Fig. B12.11 Extracranial duplex, longitudinal plane. Poststenotic
flow pattern in the V2-VA of the dominant left VA (flow velocity:
56/30 cm/s).
Fig. B12.10 Extracranial duplex, longitudinal plane. Increased flow
velocity and turbulence in the left V1-VA (peak systolic flow velocity:
93 cm/s).
Fig. B12.12 Extracranial duplex, longitudinal plane. Normal flow
signal in the right V2-VA (flow velocity: 50/25 cm/s).
Fig. B12.13 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Poststenotic flow pattern in the left M1-MCA (flow
velocity: 35/18 cm/s).
Fig. B12.14 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Poststenotic flow pattern in the right M1-MCA (flow
velocity: 40/25 cm/s).
Case 12 Bilateral Proximal Extracranial Internal Carotid Artery Occlusion and High-grade V1 Vertebral Artery Stenosis
198
Degree of Neurosonologic Difficulty: Medium
Fig. B12.15 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Poststenotic flow pattern in the left A1-ACA (flow
velocity 50/30 cm/s).
Fig. B12.17 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Raised flow velocity in the left P1-PCA indicating
collateral flow (flow velocity: 93/49 cm/s).
Fig. B12.16 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Poststenotic flow pattern in the right A1-ACA (flow
velocity: 45/30 cm/s).
Fig. B12.18 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Raised flow velocity in the right P1-PCA indicating
collateral flow (flow velocity: 90/41 cm/s).
Fig. B12.19 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Turbulent flow in the left PCoA.
Fig. B12.20 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Turbulent flow in the right PCoA (flow velocity: 76/
62 cm/s).
Final Diagnosis
199
Degree of Neurosonologic Difficulty: Medium
Fig. B12.21 DSA, aortic arch injection, posteroanterior view. Occlu-
sion of both ICAs at the level of the carotid bifurcation (arrows).
Fig. B12.23 DSA, right CCA injection, lateral view. Right extracranial
ICA occlusion (arrow).
Fig. B12.22 DSA, left CCA injection, lateral view. Left extracranial
ICA occlusion (arrow).
Fig. B12.24 DSA, left SA injection, posteroanterior view. Highgrade stenosis of the left VA at its origin (arrowhead). Note the
concomitant proximal SA stenosis.
Case 12 Bilateral Proximal Extracranial Internal Carotid Artery Occlusion and High-grade V1 Vertebral Artery Stenosis
200
Degree of Neurosonologic Difficulty: Medium
Fig. B12.25 DSA, right VA injection, posteroanterior view. Simulta-
neous filling of the MCA and PCA territory via the right PCoA. Note
the delayed arrival of the contrast media in the ACA.
Fig. B12.27 Schematic drawing of the extra- and intracranial brain
supplying arteries of the patient in Case 12. Note the bilateral ICA
occlusion and proximal lef t VA stenosis (circles). Collateral blood flow
towards the anterior circulation via both PCoAs.
Fig. B12.26 DSA, right VA injection, lateral view. Simultaneous filling of the posterior and anterior circulation through the right PCoA
(arrow).
Discussion
Clinical Aspects
Here we discuss a patient with bilateral extracranial ICA
occlusions of atherosclerotic origin (for further discussion
of unilateral ICA occlusion, see also Case 28, p. 319). As this
constellationisararefindingeveninstrokepatients,there
are no precise epidemiological data on its incidence and
prevalence. A duplex sonographic study reported a bilateral ICA occlusion in 15 of 3200 unselected patients
(0.47%) (Lazarides et al. 1991). Except for the rare cases
of abilateral ICA dissectionwhich may also lead to bilateral
ICA occlusion, most bilateral occlusions are—as in our re-
ported patient—of atherosclerotic origin. Patients demonstrate the usual known vascular risk factors. Interestingly,
very heavy smoking was prevalent in 93–10 0 % o f c ase s i n
two studies comprising a total of 95 patients, generally in
combination with at leastone additional risk factor such as
hypertension, ischemic heart disease, hyperlipidemia, or
diabetes (AbuRahma and Copeland 1998, Wade et al.
1987). Wade and coworkers reported a predominance in
the male population (91% of cases). They also reported a
14% prevalence of vertebrobasilar transient ischemic attacks (TIAs) manifested by syncope, vertigo, and drop
attacks. As these symptoms sometimes occurred in association with hyperextension of the neck or with orthostatic maneuvers, a steal phenomenon in the posterior
circulation as a result of the collateral function was suspected. The “shaking limb sign,” ararebutprototypicsign
of a hemodynamic TIA caused by ICA occlusion, however,
was observed in one of 74 patients only. Over a mean
observational period of 42 months, the medically treated
Discussion
201
patients in this study had an annual combined risk of TIA
and stroke of 15 % and a stroke risk of 13 %. The annual
mortality was 8 % (Wade et al. 1987). An even higher overall mortality was found in a smaller case series in which six
of eight (75 %) medically treated patients died during a
mean follow-up of 6 years. In contrast, only five of 13
(38%)operatedpatientsdied(AbuRhamaandCopeland
1998). In our case we primarily considered the insertion of
an EC-IC bypass (for further discussion on EC-IC bypass,
see also Case 25, p. 297). As our patient’sclinicalcondition
remained stable and he demonstrated normal cerebral
vascular resistance, we did not undertake any revascularizing measures.
In our patient there is no doubt about the hemodynamic
origin of the internal border zone lesions. The bilateral
infarctions in the region between MCA and ACA territories
could morphologically also be interpreted as embolic infarctions (for further discussion on border zone infarction,
see also Chapter 4, “Arterial Ischemia,” p. 64, and Case 30,
p. 338). However, the question remains whether the recent
left infarction really was of embolic origin. The history of
presenting complaint revealed a stepwise rather than sudden development of symptoms over a number of weeks,
including an altered behavioral state. Likewise for the
aphasia, the onset was gradual. Angiography was suggestive for old ICA occlusions, as the vessels were smooth and
rounded at the site of occlusion and no potential embolic
source such as a vascular stump could be found. As the OA
did not contribute as a collateral artery, it could not be the
embolic source. The borders between vascular territories
can be quite variable (van der Zwan et al. 1992) and the
border between ACA and MCA territory in our case might
have been shifted over time more posteriorly. However,
the final classification in our patient remains open.
An additional finding in our patient was an asymptomatic stenosis of the left VA at its origin (V0-VA segment),
which helped to confirm the underlying atherosclerotic
vascular pathology. In contrast with the ICA stenoses, little
has been published about incidence, clinical manifestation, and course of stenoses at the VA origin. Atherosclerotic changes in this location are a frequent finding. Plaque
formation often starts within the subclavian artery (SA)
and continues over several centimeters into the VA (Castaigne et al. 1973, Fischer et al. 1965). An angiographic
study that analyzed the distribution patterns of extracranial stenoses in patients with chronic stroke reported
atherosclerotic proximal ICA stenoses in 34 % of cases
and V0/V1-VA stenoses in 22 % of cases (Hass et al. 1968).
The most comprehensive register of 407 prospectively
analyzed patients with ischemic events in the posterior
circulation is the “New England Medical Center Posterior
Circulation Registry,” in which a VA stenosis > 50% near its
origin was reported in 131 patients (102 unilateral, 29
bilateral) (Caplan et al. 2004). Proximal VA atherosclerosis
is often associated with atherosclerotic vessel changes in
the intracranial VA segments and the basilar artery (BA),
and also in the anterior circulation (for further discussion
on intracranial VA pathology, see also Case 8, p.165). However patients with ischemia in the posterior circulation
may also present with only isolated proximal VA pathol-
There does not appear to be a significant difference
between the mechanisms of stroke in the anterior and
posterior circulations. Atherosclerotic lesions within the
extracranial VA commonly lead to artery-to-artery embolic events into the ipsilateral VA or the distal BA (Caplan
et al. 1992, Pessin et al. 1988). Hemodynamic events are
less frequent, which is due to the special constellation of
potential collateral pathways via the contralateral VA. Dizziness and vertigo, blurred vision, or ataxia are typical
clinical symptoms of hypoperfusion in the posterior circulation (Wityk et al. 1998). The clinical prognosis depends
on the number and efficiency of collaterals. Deep cervical
collaterals were found in 31 % of cases with proximal VA
occlusion and only in 9 % with proximal VA stenosis (Wityk
et al. 1998).
Treatment of proximal occlusive processes in the VA is
empiric and not evidence based. In analogy to proximal
carotid artery disease, antiplatelet agents are generally
used, and occasionally warfarin. Small case series report
the results of interventional therapeutic strategies with
stenting, angioplasty, or both. Good results with high procedural successrates and low periprocedural complication
rates were reported. Stenting seems not to be superior to
balloon dilatation with respect to restenosis rates but the
rate of stroke at follow-up might be lower after stenting
procedures (Cloud et al. 2003, Eberhardt et al. 2006).
Angiologic and Anatomic Aspects
Our case demonstrates that ICA occlusions are easily diagnosed by duplex ultrasound. Characteristic findings are an
absent color and Doppler flow signalalong the extracranial
ICA course. If the occlusion is located further distally, a
proximal stump signal with alternating flow with a missing diastolic flow component might be found. In a comparative study between duplex ultrasound and DSA in 91
patients with ICA occlusion, duplex ultrasound yielded
sensitivity,specificity,and positive and negative predictive
values of 91 %, 99 %, 96 %, and 98 %, respectively (AbuRahma et al. 1997). If contrast agents are used these results
might be further improved as the detection of minimal
flow within a severe stenosis, the evaluation of flow in the
presence of severely calcified plaque, and therefore the
differentiation between true and near occlusion is facilitated (Fürstetal.1999,Ohmetal.2005)(forfurtherdiscussion on ICA near occlusion, see also Case 15, p. 215).
The etiological classification in our patient was difficult
as only mild hyperechogenic atherosclerotic vessel wall
changes were found. A potential differential diagnosis
could have been a bilateral ICA dissection. However,
none of the typical dissection signs such as an intima
flap, vessel wall hematoma, or tapering occlusion were
present. The final classification of atherosclerosis was
Degree of Neurosonologic Difficulty: Medium
Case 12 Bilateral Proximal Extracranial Internal Carotid Artery Occlusion and High-grade V1 Vertebral Artery Stenosis
202
made onthe basisof the additionally detected proximal VA
stenosis.
As with all angiologic techniques, imaging of the VA
origin is more complicated than imaging of the ICA origin.
This is also true for digital subtraction angiography (DSA),
except for those cases in which the VA originates from the
cranial side of the SA, which can be observed in only about
50 % of cases. In the remaining cases the vessel originates
from the posterior, and in a minority even from the inferior
SA wall (Trattnig et al. 1993) (see also Chapter 2, “Extracranial Arteries,” p.18). In V0-VA stenosis a selective VA
angiography might not be possible and accidental catheterization of a high-grade stenosis might cause plaque
dislocation dissection or vessel occlusion. A further com-
Degree of Neurosonologic Difficulty: Medium
plicating factor might be overlapping of vessel segments.
Even if the catheter can directly be placed near the VA
origin, DSA image quality is often impaired. In a study
comparing DSA with intraoperative findings, angiography
overlooked 10 kinked regions and three stenoses at the VA
origin in a series of 30 patients with symptoms and signs of
posterior circulation ischemia (Farres et al. 1996).
Ultrasound imaging of the VA origin is, although noninvasive, similarly problematic. In routine ultrasound
commonly only the V2-VA segment is visualized as it is
easy to assess. Normal flow profiles within the V2-VA segment, however, can only confidently rule out a stenosis of
at least about 70–80%proximalordistaltotheplaceof
insonation. For asymptomatic patients this might be suffi-
cient as there are no therapeutic guidelines. However, in
patients with clinical symptoms or infarction within the
posterior circulation, the total accessible length of the
vessel should be evaluated. Our patient was asymptomatic
withrespecttotheposteriorcirculationbutdemonstrated
a poststenotic flow pattern in the left V2-VA segment,
which alone required an extended VA analysis. The search
for an underlying pathology as well as the assessment of
collaterals for the anterior circulation were additional arguments for an extended ultrasound investigation. In our
presented case, the VA origin was well accessible to ultrasound examination. However, because the vessels are frequently tortuous or kinked within this region, ultrasound
evaluation might be difficult. A direct ultrasound visualization of the VA origin may be problematic in up to 40 % of
casesontheleftandin14%ontherightside(seealso
Chapter 2, “Extracranial Arteries,” p. 18). Within the VA
origin, flow might be turbulent and the pulsatility increased without pathological relevance. Elongations lead
to difficulties in exact angle correction, which often impedes exact measurements of flow velocities within theVA
origin. Therefore, flow velocities should critically be evaluated and combined with other indirect criteria. This was
necessary in our case. The intrastenotic peak flow velocity
of 93 cm/s is still within the border zone range if a cut-off
value of 100 cm/s is considered for the V0-VA segment
(Kuhl et al. 2000). However, the clear poststenotic flow
pattern in the distal VA segments facilitated the diagnosis
of a high-grade V0-VA stenosis, which was finally con-
firmed by DSA. A recent duplex ultrasound study demonstrated sensitivity, specificity, and positive and negative
predictive values of 71%, 99 %,100 %, and 29 % respectively,
for the exclusion of V0-VA stenoses ≥ 70 % compared with
DSA, if indirect hemodynamic signs were included (de
Bray et al. 2001).
The use of MRI as an alternative imaging technique is
still quite limited. Contrast-enhanced MRA should be the
method of choice. However, even with this technique, the
accuracy for detection of a VA stenosis is still lower when
compared with the ICA origin.Thisiscausedbyfalsepositive findings as well as by the overestimation of the
degree of stenosis. Sensitivity, specificity, and positive and
negative predictive values for contrast-enhanced MRA detectionof a >50% VAstenosiswere 100%, 85%,100%, and
58 %, respectively. Analysis of other craniocervical vessels,
excluding the VA (brachiocephalic trunk, CCA, SA) yielded
values of 100 %, 98 %, 100 %, and 83 %, respectively (Randoux et al. 2003). This is particularly disappointing as the
above study applied only rough estimates of stenosis (normal, > 50 % and < 50%). A second study reported sensitivity
and specificity of 88 % and 98 % for diagnosis of occlusive
VA disorders compared with 94% and 97%, respectively,
for carotid artery disease. However, V0/V1-stenoses could
not be assessed because of motion artifacts (Yang et al.
2005). CTA is promising but its accuracy in detecting VA
pathology, especially at the VA origin where image quality
might be impaired by shoulder girdle artifacts, has not yet
been systematically evaluated (Puchner et al. 2007).
Another aspect to be considered in analysis of proximal
VA stenoses is the anatomic peculiarity that both VAs
mergetoformonedistalvessel,theBA.Inthecaseof
unilateral occlusion, the contralateral side can compensate
for the failure. However, in up to 10 % of individuals VA
diameters show considerable asymmetry. It is therefore of
great importance, if a normal or a hypoplastic VA is affected by a stenosis. In our case, both VA were equally
developed. Thus, it can be assumed that the nonaffected
right VA contributed considerably more to the overall
brain perfusion compared with the stenosed left VA.
Another potential collateral pathway in high-grade
proximal VA stenosis, not found in our patient, is a distal
filling of the VA via collaterals from the deep thyrocervical
trunk and branches of the ECA. This variant might further
complicate correct VA evaluation, not just for ultrasound
technique.
Finally, the effect of extracranial pathology on intracranial hemodynamics has to be discussed. In our case, both
anterior territories derived their blood supply via primary
collateral pathways, i. e., both PCoAs from the posterior
circulation. Accordingly, high flow velocities were found in
both P1-PCA segments. Theanatomic course of bothPCoAs
on color-mode imaging was not clearly visible, however
turbulent flow signals and raised flow velocities could be
detected. Such findings in the communicating arteries are
a sign of raised collateral flow in a relatively small vessel
althoughitcanalsobesuggestiveofastenosis.Wethere-
Discussion
203
fore call these “functional” stenoses. In cases with impaired insonation conditions, confusion of a PCoA collateral with a proximal PCA stenosis or of an ACoA collateral
with the proximal MCA or distal ICA may occur. A practical
rule of thumb is that any assumed intracranial high-grade
stenosis in extracranial ICA occlusion is most likely attributed to one of the communicating arteries until proved
otherwise. In our patient, the collateral flow via both
PCoAs was easily depicted because of the good transtemporal insonation quality. This flow pattern was also assured by the applied oscillation of the right atlas loop
which led to typical flow transients on both MCAs. In
poor transtemporal ultrasound access this test may be of
help to assess the collateral pathways. The distal PCA segments in our presented case demonstrated normal find-
ings, arguing against any relevant leptomeningeal collateralization. Likewise no retrograde OA collateral was
found. The absence of any of the above secondary collateral pathways and the only mildly poststenotic flow pattern in the ACA and MCA supported the assumption that
both PCoA diameters were large enough to provide suffi-
cient collateral perfusion toward the anterior circulation.
This was also confirmed by the normal preserved CVR
capacity. Correspondingly, the DSA demonstrated a simultaneous contrast filling of PCA and MCA. A slight delay in
the ACA filling was the only indicator of a marginal impairment of collateral circulation (for further discussion on
collateral circulation see Chapter 5, “Collateral Pathways,” p.101).
Degree of Neurosonologic Difficulty: Medium
204
Case 13
Internal Carotid Artery Stenosis in Fibromuscular Dysplasia and
Wegener Granulomatosis
Clinical Presentation
A 51-year-old woman presented with stepwise deterioration of a left hemiparesis that had started 3 days prior to
admission. The medical history revealed chronic rhinitis,
sinusitis, and bronchitis but no vascular risk factors. On
neurologic examination, the patient had a severe leftsided brachiofacial hemiparesis (National Institutes of
Health Stroke Scale [NIHSS] score 8). In addition, she had
nasal congestion.
Initial Neuroradiologic Findings
Cerebral computed tomography (CT) scan on the day of
admission revealed ischemic infarction in the anterior and
posterior territories of the right middle cerebral artery
(MCA). Magnetic resonance imaging (MRI) was not performed (Fig. B13.1).
Suspected Diagnosis
Ischemic brain infarction in the right MCA territory of
unknown origin.
Question to Answer by Ultrasound Techniques
• Was there evidence of a stenotic process, particularly in
the right internal carotid artery (ICA) or MCA?
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode sonography revealed only mild atherosclerosis of
the carotid arteries. Color imaging revealed elongation and
caliber variations of both distal ICAs, but predominantly
affecting the right side. Blood flow velocity in the proximal
right ICA was mildly reduced (flow velocity: 47/24 cm/s)
and the pulsatility mildly increased. Within the distal segment of the right ICA, a nonangle-corrected peak systolic
flow velocity of 250 cm/s was observed. Normal flow velocities were seen in the remaining extracranial vessels
(Figs. B13.2, B13.3).
Transcranial Duplex Sonography
The temporal window was inadequate for a complete insonation of the anterior circulation. Punctual signals of the
proximal M1-MCA could be obtained, revealing an obvious
flow velocity difference between the two sides (flow velocity:rightM1-MCA:57/25cm/s,leftM1-MCA:111/
55 cm/s) (not shown). The calculated Zanette asymmetry
index for the systolic velocities was 64 and the right to left
ratio (= velocity of the affected M1/normal M1 velocity)
was 0.51. Assessment of the other intracranial vessels
showed normal and symmetric flow signals.
Conclusion
Distal extracranial right ICA stenosis, approximately 70 %.
Suspected right distal M1-MCA occlusion, probably of embolic nature.
Clinical Course (1)
Thrombolysis was not indicated because of the time delay
and the signs of infarction on CT. The above vascular
changes in a young patient without classic vascular risk
factors did not favor an atherosclerotic etiology. In particular, no arterial hypertension was present. Normal 24hour ECG and echocardiography made a cardioembolic
source unlikely. There was no coagulopathy involving protein C and S, anti-cardiolipin antibodies, activated protein
C resistance and lupus inhibitor. The cerebrospinal fluid
(CSF) was normal. In view of the history of chronic rhinitis,
sinusitis, and bronchitis, specific laboratory tests were
performed which revealed an increased erythrocyte sedimentation rate (ESR) (70 mm/hr, Westergren), mild anemia, and thrombocytosis of 1200/nl (normal range:
130–340/nl), but normal white blood cell counts. In addition, the level of cytoplasmic antineutrophilic cytoplasmic
antibody (cANCA) was increased to 98 E/mL (normal:
< 15 E/mL), and urine proteins and erythrocytes were elevated. Finally, a nasal mucosa biopsy confirmed Wegener
granulomatosis (WG).
Conventional Angiography (Day 5)
DSA was performed to examine the presumed ICA stenosis
and to rule out vasculitis. Multiple irregular concentric
constrictions with normal and dilated intervening segments were found in both distal extracranial ICAs, though
predominantly affecting the right side. This “string of
beads” pattern led to the diagnosis of fibromuscular dysplasia (FMD) (Figs. B13.4, B13.5). Mild caliber variations
were also seen in the left distal vertebral artery (VA) and
the right renal artery. The intracranial vessels, in particular
the MCA branches, were not affected. Dissection or vasculitis was able to be excluded.
Clinical Course (2)
A recurrent artery-to-artery embolism from the greater
affected right ICA was assumed to be the most likely cause
of the stroke. Therefore anti-platelet therapy was commenced for secondary stroke prevention. Interventional
treatment by stenting or surgery was not recommended
because of the complex vessel pathology and WG. The WG
was treated with cyclophosphamide and corticosteroids. A
clinical follow-up 6 months after the initial presentation
showed only a minor improvement of the hemiparesis.
ESR and cANCA had normalized during the immunosuppressive therapy. Cerebral CT scan showed the residual
large ischemic MCA territory infarction (Fig. B13.6). On
Follow-up Neurosonologic Findings (5Years)
this occasion an MRI was also performed which demonstrated wallerian degeneration of the pyramidal tract up to
the pyramidal decussation (Fig. B13.7). The patient re-
mained asymptomatic over the subsequent 5 years.
Follow-up Neurosonologic Findings
(5 Years)
Extracranial Duplex Sonography
B-mode sonography revealed unchanged mild atherosclerosis of the carotid arteries. In the right CCA, a high resistance flow signal was seen. The right ECA showed an
“internalized” low resistance flow signal indicating orbital
collateral flow. Doppler spectrum analysis of the proximal
right ICA demonstrated a “stump-signal” (Figs.B13.8,
B13.9).
Transcranial Duplex Sonography
Thetranscranialbonewindowhadfurtherworsened.
Doppler spectrum analysis of the right MCA revealed a
positive effect on mild oscillation of the left ICA at the
submandibular level but not of the dominant VA at the
atlas loop. The anterior communicating artery (ACoA)
demonstrated turbulent flow. The remaining intracranial
vessels could not be visualized. The OAs were not examined.
205
Degree of Neurosonologic Difficulty: Medium
Fig. B13.1 Unenhanced CT, axial plane. Ischemic infarction in the
right anterior and posterior MCA territories (arrows). (Reproduced
from Brann et al. 2006, Fig. A, with kind permission of Springer
Science and Business Media.)
Fig. B13.2 Extracranial duplex, longitudinal plane. Normal flow signal in the right proximal ICA revealing a mildly reduced velocity and
mildly increased pulsatility (flow velocity: 47/24 cm/s).