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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
Case 15 Near Occlusion of the Extracranial Internal Carotid Artery
216
Conclusion
Near occlusion of the left ICA below the OA origin. There
was collateral blood flow for the left ACA, MCA, and PCAvia
the anterior communicating artery (AcoA) and retrograde
OA. Also, a left fetal-type PCA was present.
Conventional Angiography
Digital subtractionangiography (DSA) of the brain-supplying arteries, kidney arteries, and coronary arteries was
performed. The left carotid injection confirmed the segmental narrowing of the CCA and demonstrated a prox-
Degree of Neurosonologic Difficulty: Medium
imal near occlusion of the ICA with a secondary longsegmental narrowing up to the petrous segment of the
ICA. There was delayed contrast filling of the MCA and PCA
territory and no filling of the ACA territory. Only a mild
collateral blood flow could be detected via the OA. Furthermore, a left fetal-type PCA was confirmed. The right
carotid injection showed cross-flow to the left side causing
a mildly delayed filling of the left ACA and MCA. Selective
aortic and coronary angiograms revealed high-grade
aortic isthmus stenosis and stenosis of two coronary arteries (Figs. B15.17–B15.21).
Fig. B15.22 shows a schematic drawing of the extra- and
intracranial brain-supplying arteries of the patient.
denceofrestenosis.ThemoderateCCAstenosisremained
unchanged (Fig. B15.23).
Transcranial Duplex Sonography
Left MCA, ACA, and PCA segments as well as the left OA
demonstrated normalized flow signals (Figs. B15.24,
B15.25).
Conclusion
Left ICA after local stent insertion without residual stenosis. The intracranial circulation had normalized. The moderate left CCA stenosis remained unchanged.
Clinical Course (2)
Three months after ICA intervention, a stent was inserted
into the aortic isthmus stenosis. The intervention was
successful and the ankle-brachial index improved from
0.7 to 1.0 on both sides. To date, there have been no
more ischemic attacks.
Follow-up Neurosonologic Findings (5 Months)
Clinical Course (1)
In the present patient, we considered the etiology of the
ICA and coronary isthmus stenoses to be of atherosclerotic
origin, which was probably caused by long-term arterial
hypertension of the upper systemic circulation secondary
to high-grade aortic stenosis. The initially elevated ESR
normalized spontaneously during the subsequent few
days, further arguing against inflammation or arteritis.
During the patient’s stay in the hospital, she experienced
two more TIAs with episodes of right-sided hypesthesia of
the hand and arm despite the absence of blood pressure
reduction, supporting the hypothesis of recurrent embolic
events. It was decided to treat both of the stenoses by a
two-step interventional stent implantation, beginning
with the left ICA. The first stenting proceeded uneventfully
and the patient was again given aspirin and clopidogrel for
2 months. No further ischemic events occurred.
Follow-up Neurosonologic Findings (2 Months)
Extracranial Duplex Sonography
Doppler spectrum analysis showed a normalized left carotid flow, including the stented ICA segment without evi-
Extracranial Duplex Sonography
Doppler spectrum analysis within the left ICA stent demonstrated a long segmental increase of flow reaching
177 cm/s peak systolic flow velocity (Fig. B15.26).
Transcranial Duplex Sonography
Intracranial findings had remained unchanged.
Conclusion
Restenosis of the left proximal ICA, approximately
60–70 %.
Final Diagnosis
Multiple brain infarctions mostly of embolic origin within
the left MCA, ACA, and ICA-dependent PCA territory
causedbynearocclusionoftheleftICAonthebaseofa
severe generalized atherosclerosis. This was secondary to
arterial hypertension in the upper systemic circulation in
aortic isthmus stenosis. There was restenosis in the left ICA
of 60–70 %, 5 months after stent implantation. No reintervention was performed and treatment with clopidogrel
continued. No further progression was noted during the
4-year follow-up.
Final Diagnosis
217
Degree of Neurosonologic Difficulty: Medium
Fig. B15.1 MR T2-weighted image, axial plane. Multiple small hy-
perintensities in the left ACA, MCA, and PCA territories consistent
with multiple ischemic lesions (arrows).
Fig. B15.3 Intracranial 3D TOF MRA, coronal MIP. Absent signal in
the left ICA and the left PCA.
Fig. B15.2 MR FLAIR-weighted image, sagittal plane. Multiple small
hyperintensities in the left ACA, MCA, and PCA (arrowhead) territories, consistent with multiple mostly embolic ischemic lesions.
Note also the affliction of the basal ganglia (arrow).
Fig. B15.4 Extracranial duplex, longitudinal plane. B-mode imaging
of the left CCA shows a moderate lumen reduction caused by a
homogeneous mild hyperechogenic plaque.
Case 15 Near Occlusion of the Extracranial Internal Carotid Artery
218
Degree of Neurosonologic Difficulty: Medium
Fig. B15.5 Extracranial duplex, longitudinal plane. Doppler spec-
Fig. B15.7 Extracranial duplex, longitudinal plane. Left ICA with a
Fig. B15.6 Extracranial duplex, longitudinal plane. Left ECA shows a
Fig. B15.8 TCCS (transtemporal approach), left-sided insonation,
Fig. B15.9 TCCS (transtemporal approach), left-sided insonation,
Fig. B15.10 TCCS (transtemporal approach), left-sided insonation,
Final Diagnosis
219
Degree of Neurosonologic Difficulty: Medium
Fig. B15.11 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Normal flow in the right M1-MCA (peak systolicflow
velocity: 114cm/s).
Fig. B15.13 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Functional stenotic flow signal in the ACoA caused
by intracranial cross-flow.
Fig. B15.12 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Turbulent and reversed flow in the left A1-ACA (flow
velocity: 75/40 cm/s).
Fig. B15.14 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Increased flow in the right A1-ACA, indicative of
collateralization (flow velocity: 164/104 cm/s).
Fig. B15.15 TCCS (transorbital approach), left-sided insonation:
Raised retrograde flow in the left OA with an internalized flow
pattern (flow velocity: 70/35 cm/s).
Fig. B15.16 TCCS (transorbital approach), right-sided insonation:
Normal and orthograde flow in the right OA (flow velocity: 25/
5cm/s).
Case 15 Near Occlusion of the Extracranial Internal Carotid Artery
220
Degree of Neurosonologic Difficulty: Medium
Fig. B15.17 DSA, left CCA injection (early arterial phase), lateral
view. Near occlusion of the left ICA caused by a proximal stenosis
(arrows). Note the long-segment poststenotic lumen reduction up
to the petrous part of the ICA caused by the reduced flow (arrowheads). Note a small contrast blush in the OA filled by the maxillar y
artery (single arrow).
Fig. B15.18 DSA, left CCA injection (late arterial phase), lateral view.
Note the delayed filling of the distal carotid (arrows) and of the MCA
(arrowhead).
Fig. B15.19 DSA, left CCA injection, posteroanterior view. Delayed
MCA and PCA filling in contrast to the filling of peripheral ECA
branches (arrowheads). No filling of the left ACA. Note the left-sided
fetal-type PC A (arrows).
Fig. B15.20 DSA, right CCA injection (early arterial phase), posteroanterior view: Note the good but slightly delayed filling of the left
MCA territory from the right ICA via ACoA and retrograde A1-ACA
(cross-flow).
Final Diagnosis
221
Degree of Neurosonologic Difficulty: Medium
Fig. B15.21 DSA, left VA injection, posteroanterior view. No filling of
the left PCA territory indicating a left-sided fetal-type PCA. Note the
absent collateral flow to the anterior circulation.
Fig. B15.23 Extracranial duplex, longitudinal plane. Doppler spectrum shows normal flow in the stented left ICA (flow velocity: 77/
36 cm/s).
Fig. B15.22 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 15. Note the near occlusion
of the left proximal ICA (circle). Collateral blood flow mainly via the
right side through ACoA and retrograde left A1-ACA. There is additional collateral flow from the left ECA and retrograde OA toward the
left anterior and posterior circulation. Note the left fetal-type PCA
anatomic variant.
Fig. B15.24 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normalized flow signal in the left M1-MCA following
stenting of the left ICA (flow velocity 115/50 cm/s).
Case 15 Near Occlusion of the Extracranial Internal Carotid Artery
222
Degree of Neurosonologic Difficulty: Medium
Fig. B15.25 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normalized flow direction in the left A1-ACA segment (flow velocity: 85/35 cm/s).
Discussion
Clinical Aspects
Here we present a 42-year-old patient who experienced
multiple ischemic infarctions in the left hemisphere,
which were considered to be of embolic and hemodynamic origin (for further discussion on BZI, see also Chapter 4, “Arterial Ischemia,” p.64,andCase30,p.338).The
underlying cause was a near occlusion of the proximal ICA
(synonym: pseudoocclusion, subocclusion, critical stenosis, preocclusive stenosis, incomplete occlusion) with subsequent poststenotic ICA narrowing and “string sign.” The
etiology of the stenosis was considered to be atherosclerosis, promoted by a high-grade aortic isthmus stenosis
and subsequent upper systemic arterial hypertension. As
no other classic vascularrisk factors could be found, hypertension was considered to be the essential trigger of the
disease. The initially raised ESR in combination with the
young age of our patient was suggestive of vasculitis, e. g.,
Takayasu arteritis. However, ultrasound clearly revealed
extended atherosclerotic vessel wall changes and no signs
of vasculitis (for further discussion on Takayasu arteritis,
see Case 23, p. 279).
The treatment options for symptomatic and asymptomatic ICA stenoses are extensively discussed in Case 1
(p.128). Here we focus on the treatment options of ICA
near occlusions. There is no doubt that patients with a
symptomatic high-grade stenosis of 70–99 % (according
to North American Symptomatic Carotid Endarterectomy
Trial [NASCET] criteria) benefit distinctly and those with a
50–69 % stenosis benefit moderately from revascularization by carotid endarterectomy (CEA) (Rothwell et al.
2003a, b). The stroke risk has been shown to increase
with the grade of stenosis, which initially led to the assumption that near occlusions, defined as an ICA/CCA ratio
Fig. B15.26 Extracranial duplex, longitudinal plane. Restenosis of
the left ICA with long segmental increase of flow velocity (flow
velocity: 177/66 cm/s).
< 0.42, carry the greatest risk. The NASCET study did find a
benefit for CEA in these patients which was, however,
distinctly smaller than for the high-grade stenoses (Barnett et al. 1998). The European Carotid Surgery Trial (ECST
1998) could not confirm this finding. An analysis of pooled
data from three main CEA trials (ECST, NASCET, and VA309)
comprising 6092 patients finally revealed a nonsignificant
trend in favor of CEA over medical treatment. However,
this was only found at the 2-year follow-up and the trend
disappeared after 5 years (Rothwell et al. 2003a). The
perioperative risk in the CEA group was low but at the
same time the stroke risk in the medically treated patients
with near occlusion was found to be similarly low (Morgenstern et al. 1997). It has been speculated that near
occlusions are far less likely to cause embolic events because of the poststenotic lumen reduction and the small
residual proportion of blood flowing into the dependent
hemisphere. The latter can be confirmed by digital subtraction angiography (DSA), which often demonstrates a
distinctly delayed contrast filling of the affected ICA as well
as the presence of collateral pathways (Rothwell and Warlow 2000). In the NASCETstudy, the collateral function was
an important predictor of subsequent cerebral ischemia, in
particular for the 85–99% stenoses. In contrast, patients
with near occlusion had a lower risk of stroke comparable
to low-grade stenoses, which was relatively unrelated to
the collateral vessel status (Henderson et al. 2000, Rothwell and Warlow 2000). Based on the current available
data a general recommendation of CEA in symptomatic
near occlusion cannot be given. In instable disease a revascularization may be indicated in patients with recurrent ischemia despite best medical treatment and if the
cerebral vascular resistance is exhausted.
The current general recommendation is medical treatment with antiplatelet agent. However, our patient remained symptomatic under medical treatment. Because
Discussion
223
of the monomorphic character of clinical symptoms, a
hemodynamic cause was likely. Interventional percutaneous transluminal angioplasty and stenting was performed,
after which our patient remained clinically asymptomatic
but developed a 60–70 % restenosis after 5 months. Without further intervention the stenosis remained unchanged
over 4 subsequent years.
Successful stent placement in near occlusion of the ICA
hasbeenreportedoninsmallcaseseries.Teradaand
coworkers performed stenting of near occlusion in 20
patients, 17 of whom were symptomatic. The mean grade
of stenosis was reduced from 95 % to 6.7 %. The authors
found no postinterventional ischemia over an observational period of 25 months but one restenosis, which was
treated by repeated stenting (Terada et al. 2006).
A metaanalysis including 34 studies and 4185 patients
evaluated restenosis rates after PTA and stenting. Defining
a vessel narrowing ≥ 50 % as restenosis the cumulative rate
after 1 year was 6 % and after two years 7.5 %, indicating a
dominance of early restenosis (Gröschel et al. 2005). Systematic long-term follow-up data are not yet available.
Angiologic and Anatomic Aspects
A near occlusion describes a partial collapse of a vessel due
to a proximal high-grade stenosis. A progressing ICA
stenosis initially demonstrates raised flow velocities
within the stenosis to maintain blood volume flow. In a
critical grade of stenosis (> 90 %), sufficient blood flow
cannot be ensured and the vessel lumen decreases. Initially raised peak systolic flow velocities, up to a maximum
of 500 cm/s, quickly decrease first into the normal range
and subsequently to a small residual flow (see also Chapter 5, “Stenoses and Occlusions,” p. 81). Even if the primary collateral pathways are activated, a residual ICA flow
may persist but may not relevantly contribute to the perfusion of the brain but of the eye. If the stenosis continues
to increase or the OA flow becomes retrograde to contribute as further collateral, perfusion pressure may become
critically low. This was the case in our patient, who demonstrated a very small orthograde flow throughout the ICA
without a diastolic flow component. Furthermore, the internalized ECA flow profile was also suggestive of retrograde OA flow, which was then confirmed during transorbital insonation. The OA Doppler spectrum demonstrated a reduced pulsatility, corresponding to an artery
supplying the brain and not the eye. The ICA integrity in
the carotid siphon could be confirmed by the small residual flow detected in this region. The additional OA involvement implies an insufficient collateral flow via the anterior
communicating artery (ACoA) alone, which might also be
explainedby theneed toprovide blood flownot onlyto the
ACA and MCA but also the ipsilateral PCA territory because
oftheleftfetal-typePCA.Thecombinedcollateralflow
seemed therefore not to be adequate as the MCA and PCA
flow profiles had a moderately poststenotic flow pattern.
As expected, a moderate turbulence was seen from the
ACoA but also additionally from the retrograde left A1-ACA
segment. A possible explanation for this phenomenon is a
continuationoftheACoAturbulenceor,inourcasemore
probable, a nonpathologic vessel narrowing of the left A1ACA segment. The raised flow velocity in the right orthograde A1-ACA segment is due to the compensatory raised
collateral blood volume flow. Flow is often nonturbulent
except for cases in which the A1-ACA is small, e. g., it is
hypoplastic. A helpful indirect indicator of collateral flow
via the ACoA is the comparison of A1-ACA and MCA flow
velocities of the unaffected side. If the A1-ACA flow velocity is greater then the M1-MCA flow velocity, a cross-flow
via the ACoA can be suspected (for further details, see also
Chapter 5, “Stenoses and Occlusions,” p. 81, “Collateral
Pathways,” p.101). In cases with insufficient insonation
of the A1-ACA segment, for example due to an impaired
transtemporal bone window, a simple oscillation test may
help. Oscillation of the contralateral submandibular extracranial ICA, of the dominant V3-VA segment or the
eye bulb under continuous monitoring of the M1-MCA
profile of the affected side, allows indirect evaluation of
the presence of collateral pathways (see also Chapter 2,
“Intracranial Arteries,” p. 24).
The angiographic determination of the grade of stenosis
following the NASCET criteria in near occlusions is impaired as the necessary distal diameter cannot exactly be
determined because of the poststenotic vessel collapse. As
thenarrowestdiameterwithinthestenosisisassessedin
relation to the distal ICA diameter, near occlusions will
always result in an underestimation of the true grade of
stenosis. An ICA/CCA ratio < 0.42 is now well accepted to
define ICA near occlusion. Other criteria are based on
delayed ICA filling and delayed filling of its branches, as
well as the presence of collateral pathways. Differences in
diameter between the ipsi- and contralateral ICA as well as
ipsilateral ICA and ECA are further indicators. If two or
more of the above criteria are present, the sensitivity and
specificity of detection of a near occlusion is 90.6 % and
93.8 %, respectively (Fox et al. 2005).
DSA has been the method of choice in differentiating
between occlusion and near occlusion. Depending on the
technique used, ultrasound has a comparable accuracy.
Fürst and coworkers analyzed ultrasound and TOF MRA
derived findings of 20 patients with angiographically determined near occlusions (Fürst et al. 1999). Simple colormode duplex sonography yielded a sensitivity and specificity of 70 % and 92 % respectively. The additional use of
echo-contrast agents improved these values to 83 % and
92 %. If power-mode insonation was used alone or in combination with an echo-contrast agent, a sensitivity and
specificity of 95 %/94 % and 92 %/100 %, respectively, was
achieved. However, the authors did not analyze the Doppler flow pattern, which can be even more sensitive than
the color-mode imaging concerning low-flow situations.
Herewith, the above results couldprobably even be further
improved. Analysis of the Doppler spectrum is essential for
any ultrasound investigation. With or without echo-con-
Degree of Neurosonologic Difficulty: Medium
Case 15 Near Occlusion of the Extracranial Internal Carotid Artery
224
trast agents the detection of minimal flow beyond a severe
stenosis assures a near occlusion (Ohm et al. 2005). It also
allows the detection of rare cases such as inspiration-dependant anterograde flow within the stenosis, which turns
into zero flow during expiration. This might otherwise be
interpreted as an occlusion. None of the other techniques
would be able to detect such a subtlety. However, a limiting factor may be a distinct calcification with effacement of
the ultrasound beam impeding a clear evaluation. In this
condition an additional echo-contrast application might
facilitate the examination (Ohm et al. 2005).
TOF MRA should not be applied for analysis of near
occlusion because of its low sensitivity of 47 % (3D) and
65 % (2 D) while the specificity was 89 % (3D) and 100 %
Degree of Neurosonologic Difficulty: Medium
(2 D) (Fürst et al.1999). Contrast-enhanced MRA is now the
standard MRI technique for evaluation of extracranial occlusive ICA disease (Yang et al. 2005). In small series analyzing the accuracy of contrast-enhanced MRA compared
to DSA, all extracranial near occlusions of the ICA were
detected (Remonda et al. 1998).
CTA seems to replace DSA as standard method in near
occlusion of the ICA. Thus far, published results concerning
near occlusions are excellent. In a series of 20 patients, a
comparison with DSA yielded a sensitivity and specificity
of 100 % (Chen et al. 2004a). Other authors have reported
sensitivity ranging from 90 % to 97 % and specificity rangingfrom84%to90%(Bartlettetal.2006).Theresultsseem
to depend on the post-processing technique used. Evaluation of the source scans in axial view and additional evaluation of dots of the intraluminal contrast material may
increase the diagnostic sensitivity (Lev et al. 2003). A
common standardized technique has yet to be developed.
In conclusion, because of the illustrated potential problems and pitfalls, it is often sensible to combine different
techniques in the evaluation of near occlusions. However,
therapeutic opportunities only arise if impaired collateral
function or recurrent clinical symptoms attributable to the
stenosis are present.
Case 16
Giant-cell Arteritis with Bilateral Intracranial V4
Vertebral Artery Stenosis
225
Clinical Presentation
A 71-year-old man presented with recurrent episodes of
vertigo, dizziness, double vision, and gait disorder, each
lasting a few minutes, for the 3 weeks prior to admission.
The patient had a history of giant cell arteritis that had
been diagnosed 3 months prior to this presentation by
temporal artery biopsy. At the time he had complained
of right-sided temporal headache with jaw claudication,
masseter pain, and abnormal fatigue. Laboratory findings
revealed an increased erythrocyte sedimentation rate
(ESR) (75 mm/hr, Westergren) and an elevated C-reactive
protein (CRP) of 57 mg/L (normal < 5 mg/L). He had been
treated with high-dose steroids for 3 weeks. This was
subsequently reduced to a daily dose of 7.5 mg prednisolone. He had known vascular risk factors of arterial hypertension and a positive family history of stroke.
On admission, his neurologic examination was normal.
He had no complaints suggestive of giant cell arteritis, in
particular no headaches or jaw claudication. The ESR was
normal during treatment, but CRP levels were still slightly
raised (1.9 mg/dL).
Initial Neuroradiologic Findings
Cerebral computed tomography (CT) on the day of admission was normal. There was no evidence of brain ischemia.
CT angiogram revealed bilateral filiform stenosis of the
vertebral artery (VA) at the intradural entrance, more pronounced on the right side. Also a calcified plaque became
visible in the distal right V4-VA segment (Fig. B16.1).
Suspected Diagnosis
Recurrent TIAs in the vertebrobasilar territory due to bilateral VA stenosis at the V3-V4 junctionof unknown origin.
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
The carotid arteries showed mild atherosclerotic vascular
changes with small hyperechogenic plaques in both carotid bifurcations. The diameter in both V2-VA segments
was within normal range (left: 3.2 mm; right: 3.6 mm).
Doppler spectrum analysis demonstrated normal flow signals in the left V2-VA segment. A high-resistance flow
signal with reduced flow velocity (29/6 cm/s) was observed in the right V2-VA segment (Figs.B16.2–B16.5).
Assessment of a branch of the right STeA showed reduced color filling and a hypoechogenic vessel wall thickening consistent with a dark halo sign (Fig. B16.6). No
stenoses were seen in the main stem of the STeA and other
branches of the ECA.
Transcranial Duplex Sonography
A poststenotic flow pattern was detected in both P1- and
P2-PCA segments. The left proximal V4-VA segment revealed a turbulent flow with increased flow velocities
reaching 230/121cm/s. Flow in the right proximal V4-VA
segment was also turbulent and the velocity was raised
but no precise measurement was possible. The distal parts
ofbothV4-VAsegmentsaswellasthebasilarartery(BA)
could not be clearly detected. The anterior circulation was
normal (Figs. B16.7–B16.9).
Conclusion
Right-pronouncedbilateral high-grade VA stenosis(right >
left) within the proximal intracranial V4 segments leading
to a poststenotic flow pattern in both PCAs. Sonographic
confirmation of the temporal arteritis in the right STeA.
Clinical Course (1)
Questions to Answer by Ultrasound Techniques
• Were there signs of vasculitis or atherosclerosis in the
brain-supplying arteries or in the external carotid artery
(ECA), superior temporal artery (STeA), or STeA
branches?
• What was the degree of the bilateral distal VA stenosis?
The neurological symptoms of the patient were evaluated
as recurrent vertebrobasilar TIAs probably of hemodynamic origin and attributed to the bilateral VA stenoses.
Their etiology was thought to be either of atherosclerotic
origin or caused by the known giant cell arteritis. The
location of the stenoses at the level of the dural passage
and the symmetric pattern seemed atypical for a classic