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Case 24 Dissection of the Extracranial Internal Carotid Arter y and Contralateral M1 Middle Cerebral Arter y Stenosis
296
ICA occlusion only provided blood flow into the MCA
territory while selective filling of the contralateral ICA
revealed a blood flow from the ACoA into the ACA and
MCA. This “task sharing” may be observed, provided that
more than one collateral pathway exists. Collateral flow to
theA1-ACAsegmentontheoccludedsideisthenprovided
mainly via the contralateral A1-ACA segment, and flow
into the M1-MCA segment of the occluded side is mainly
via the ipsilateral PCoA. The positive reaction of the MCA
signal ipsilateral to the occlusion to oscillation of the VA
and contralateral ICA demonstrated the patency of both
the ACoA and the PCoA collaterals. In our case, it has to be
further assumed that the A1-ACA segment of the non-
Degree of Neurosonologic Difficulty: High
occluded ICA side did not only provide blood to the contralateral side but also via leptomeningeal anastomoses to
the ipsilateral MCA territory to compensate for the hemodynamically relevant ipsilateral M1-MCA stenosis, which
may explain the unusual high flow velocities of 225/
140cm/s. Remarkably, the MCA profile on the side of the
ICA occlusion was normal without signs of hemodynamic
impairment, indicating balanced intracranial hemodynamics. DSA correspondingly showed simultaneous filling
of both MCAs. This constellation may help to explain the
benign clinical course without the occurrence of embolic
or hemodynamically related ischemia over many years.
Another remarkable point is the morphologic evolution
of the extracranial ICA dissection as seen in DSA (see
Fig. B24.22). Initially, the conica-shaped stenosis and the
“string sign” (B) confirmed the diagnosis of a dissection.
Six months later, DSA demonstrated a rounded stump (C).
A rounded vessel end is commonly considered to be typical of atherosclerotic ICA occlusions but it may appear in
residual stages of ICA dissections (Houser et al. 1984). This
implies that a rounded ICA occlusion cannot be considered
as pathognomonic of atherosclerotic origin and a chronic
state following dissection is a relevant differential diagnosis.
Intracranial TOF MRA revealed the known limitations,
such as exaggerating the extent of MCA vessel pathology.
The presence of distal M2-MCA branches, however, argued
in favor of stenosis and against an occlusion. The weak
signal of the contralateral intracranial ICA suggested a
reduced flow, later attributed to the detected dissection.
Looking for vessel signals on conventional MRI images
may be helpful. As in the assessment of venous thrombosis, a missed signal void of arterial vessels might indicate
flow obstruction. In our case the distinct reduction of
carotid flow was easily seen in the axial T2-weighted
image (see Fig. B24.6). Also, the prominent right PCoA,
not visualized in the TOF MRA (see Fig. B24.7), was visualized without a problem in the axial T2-weighted image
(see Fig. B24.5). For ultrasound users, we recommend always using the information provided by the other angiologic techniques to improve interpretation of the study
results.
Case 25
Progressive M1 Middle Cerebral Artery Occlusion
297
Clinical Presentation
A 31-year-old woman was referred to our hospital with a
transient mild paresis of the left arm lasting for 6 hours.
Oneyearagoshehadbeenadmittedtoadistrictgeneral
hospital with a left-sided brachiofacial hemiparesis. This
had completely resolved within 4 weeks. Cerebral magnetic resonance imaging (MRI) at that time showed multiple right-sided signal abnormalities, which were considered to be ischemic embolic lesions within the middle
cerebral artery (MCA) territory (Fig. B25.1). Transcranial
duplex sonography at that presentation revealed a right
proximal high-grade MCA stenosis which was then confirmed by digital subtraction angiography (DSA)
(Fig. B25.2). She had multiple vascular risk factors including arterial hypertension, nicotine misuse, hyperlipidemia,
obesity, and she used an estrogen-containing contraceptive. An embolic source had not been detected and she was
given clopidogrel for long-term stroke prevention.
Initial Neuroradiologic Findings
Cerebral MRI on the day of this admission revealed the
known old ischemic lesions which were partly territorial
MCA infarction and partly internal and external border
zone infarctions (Fig. B25.3). There was no evidence of
any new ischemic brain lesions. Secondary widening of
the anterior horn of the right lateral ventricle was observed.
Initial Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
B-mode imaging did not reveal any atherosclerotic vascular changes. Doppler spectrum analysis showed normal
and symmetric flow signals with no difference in the pulsatility of the extracranial internal carotid arteries (ICAs)
(Figs. B25.4, B25.5).
Transcranial Duplex Sonography
ThedistalICAandthecarotidsiphonshowednormalflow
signalsonbothsides.TheleftproximalM1-MCAsegment
revealed a mildly stenotic flow pattern (flow velocity: 181/
83 cm/s). Normal signalswere observed in the corresponding M2 branches. The complete right M1-MCA segment
could well be visualized using the color-mode. Doppler
flow analysis revealed markedly reduced velocities without turbulence but with a mild poststenotic flow pattern
throughout its entire length (flow velocity: 17/10 cm/s).
Doppler spectrum analysis of the left A1 anterior cerebral
artery (ACA) segment was normal (flow velocity: 110/
68 cm/s). The right A1-ACA segment revealed a mildly
increased non-turbulent flow (flow velocity: 156/84 cm/
s). The flow velocity in the right P2 posterior cerebral
artery (PCA) segment was also mildly increased (flow velocity: 105/57 cm/s) when compared with the left side
(flow velocity: 61/25 cm/s). Also, a right-sided fetal-type
PCA was seen (Figs. B25.6–B25.11).
Suspected Diagnosis
Right hemispheric transient ischemic attack (TIA) of embolic or hemodynamic origin caused by high-grade stenosis of the right M1-MCA segment, which had been detected 1 year before.
Questions to Answer by Ultrasound Techniques
• What was the status of the brain-supplying arteries?
• What was the status of the right MCA stenosis?
• Were there any potential collateral pathways?
Conclusion
Bilateral stenoses of the M1-MCA segments. Near occlusion on the right sidewith leptomeningeal collaterals from
the right ACA and PCA. Mild M1-MCA stenosis on the left
side.
Conventional Angiography (Day 4)
DSA was performed to clarify the suspected intracranial
pathology. Significant progression was found in comparison with the DSA performed 14 monthspreviously. A near
occlusion of the right M1-MCA segment was confirmed
and leptomeningeal collateralization was seen via the
Case 25 Progressive M1 Middle Cerebral Artery Occlusion
298
right ACA and PCA. No caliber variations were seen in the
left MCA. There were no signs of vasculitis or fibromuscular dysplasia (Figs. B25.12– B25.14).
Clinical Course (1)
The new transient ischemic event was thought to be of
hemodynamic origin. The pathogenesis of the progressive
right M1-MCA stenosis was unclear. A cardiac or artery-toartery embolism was unlikely. Thrombophilia, vasculitis,
andautoimmunediseasehadbeenruledout.Theyoung
age of the patient, the rapid progression of the stenosis,
Degree of Neurosonologic Difficulty: High
and the normal vessel wall findings in the extracranial
carotid arteries argued against atherosclerotic stenosis
despite the presence of multiple vascular risk factors.
Moyamoya disease was discussed but seemed unlikely
because of the rapid progression of vessel disease and
the spared terminal ICA on both sides.
Xenon computed tomography (CT) following acetazolamide infusion revealed diminished cerebrovascular reactivity on the effected side. Because of the rapid progression
and the recurrent symptoms as well as the limited hemodynamic reserve, a superior temporal artery (STeA)–MCA
bypass was performed and long-term stroke prevention
with clopidogrel was continued.
Clinical Course (2) and Follow-up Neuroradiologic Findings
Follow-up Neurosonologic Findings (10 Months)
Extracranial Duplex Sonography
Again, all extracranial signals were normal (not shown).
Transcranial Duplex Sonography
The systolic flow velocity of the left M1-MCA segment
remained slightly increased (176 cm/s). Again, mildly
raised flow velocities were observed in the right sided
A1-ACA segment and the main stem of the PCA, suggestive
of leptomeningeal collateral function. No flow was detected within the right M1-MCA segment in spite of the
optimal insonation conditions through the right-sided
trepanation defect. There was a venous signal present in
the lateral fissure only, corresponding with the deep middle cerebral vein (Fig. B25.18).Anormalflowsignalwas
seen in the main stem of the right STeA. The STeA–MCA
bypass could not be visualized (not shown).
Conclusion
Further progression of the right-sided MCA pathology now
considered as main stem occlusion with leptomeningeal
collateral blood flow from the ACA and PCA. Unchanged
mild stenosis of the left proximal M1-MCA segment. Occlusion of the right STeA–MCA bypass.
DSA immediately after surgery showed patent collateral
vessels (not shown). Cerebral CTrevealednointracranial
bleeding and no new ischemic brain lesion (not shown).
Three months later the patient presented with a new TIA
affecting the contralateral side with sensory disturbances
in the right arm and additional headaches. Cerebral MRI
showed no evidence of new ischemic lesionsbut showed a
chronic right frontal subdural hematoma (Fig. B25.15).
Furthermore, magnetic resonance angiography (MRA)
was indicative of an occlusion of the right M1-MCA
segment and a mild stenosis of the left distal M1-MCA
segment (Fig. B25.16). Clopidogrel was stopped and the
hematoma successfully treated by a burr-hole craniotomy.
A follow-up CT after surgery was unremarkable (Fig.
B.25.17).
Clinical Course (3)
A follow-up DSA was performed, which confirmed the
occlusion of the STeA–MCAbypassaswellasthecomplete
occlusion of the right M1-MCA segment (not shown). As
the patient had now remained stable, no second bypass
operation was planned. Because of the contralateral transient brain ischemia, progression of right-sided MCA pathology and the failure of stroke prevention with clopidogrel, oral anticoagulation with phenprocoumone was
started. During the clinical and MRI follow-up over 2 years,
no new ischemic event was reported.
Figure B25.19 shows a schematicdrawing of the extra- and
intracranial brain-supplying arteries of the patient.
Final Diagnosis
Recurrent cerebral ischemia in both MCA territories
caused by a progressiveright MCA stenosis with secondary
occlusion and stable mild stenosis of the left M1-MCA
segment of unknown origin. Secondary occlusion of the
right-sided STeA-MCA bypass.
Final Diagnosis
299
Degree of Neurosonologic Difficulty: High
Fig. B25.1 MR FLAIR image, axial plane. A Multiple right hemi-
spheric signal abnormalities, consistent with a large basal ganglia
embolic ischemia and anterior and posterior external border zone
infarction (arrows). B Internal border zone infarction at the cella
media level (arrow) in addition to partial inhomogeneous territorial
MCA infarction (courtesy of Dr. Schröter, Radiologische Praxis am
Krankenhaus Rüdersdorf, Rüdersdorf, Germany).
Fig. B25.3 MR FLAIR image, axial plane. A Shrunken ischemic lesions in the right hemisphere. Enlarged right frontal horn, secondary
to the adjacent ischemic defect. B Mildly enlarged ventricles. Note
the residual external anterior border zone infarction (arrow).
Fig. B25.2 DSA, right ICA injection, posteroanterior view. Highgrade right M1-MCA stenosis (arrows). Note the concomitant filling
ofthefetal-typePCA(singlearrow)(courtesyofDr.Schröter, Radi-
ologische Praxis am Krankenhaus Rüdersdorf, Rüdersdorf, Germany).
Fig. B25.4 Extracranial duplex, longitudinal plane. Normal flow signal in the left ICA (flow velocity: 45/21 cm/s). Note a normal PI of
0.84.
Case 25 Progressive M1 Middle Cerebral Artery Occlusion
300
Degree of Neurosonologic Difficulty: High
Fig. B25.5 Extracranial duplex, longitudinal plane. Normal flow sig-
nal in the right ICA (flow velocity: 49/34 cm/s). Note a normal PI of
0.76.
Fig. B25.7 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Severely reduced flow without turbulence in the
right M1-MCA (flow velocity: 17/10).
Fig. B25.6 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Mildly increased and turbulent flow in the left M1MCA (flow velocity: 181/83 cm/s).
Fig. B25.8 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow in the left A1-ACA (flow velocity:
110/68 cm/s).
Fig. B25.9 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Strong flow signal in the right A1-ACA, indicating
leptomeningeal collateralization (flow velocity: 156/84).
Fig. B25.10 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow signal in the left proximal P2-PCA (flow
velocity: 61/25 cm/s).
Final Diagnosis
301
Degree of Neurosonologic Difficulty: High
Fig. B25.11 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Increased flow in the right proximal P2-PCA, indicating leptomeningeal collateralization (flow velocity: 105/57 cm/s).
Fig. B25.13 DSA, right ICA injection, lateral view. Markedly reduced
contrast filling of the right MCA (arrows). Note the fetal-type PCA
(arrowhead).
Fig. B25.12 DSA,rightICAinjection,posteroanteriorview.Longsegmented near occlusion of the right M1-MCA (arrows). Note the
leptomeningeal collaterals from the ACA and PCA (arrowheads).
Fig. B25.14 DSA, left ICA injection,posteroanterior view. In contrast
with the TCCS findings there is no visible stenosis of the left M1MCA.
Case 25 Progressive M1 Middle Cerebral Artery Occlusion
302
Degree of Neurosonologic Difficulty: High
f Fig. B25.15 MR T2-weighted image, axial plane. Right frontal
subdural hematoma.
Fig. B25.16 3D TOF MRA, coronal MIP. Absent signal in the right
MCA suggesting occlusion. Note a circumscribed decrease of signal
intensity in the left proximal M1-MC A indicative of stenosis (arrowhead).
f Fig. B25.17 Unenhanced cranial CT: No signs of bleeding and no
new ischemic brain damage post surgery.
Fig. B25.18 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Insonation of the right deep middle cerebral vein
whichparallelsthecourseoftheM1-MCA.Notetheabsentflow
signal of the right M1-MCA.
Discussion
Clinical Aspects
Here we report a 31-year-old woman who had recurrent
cerebral ischemia because of bilateral MCA stenosis. The
right sidedemonstrated rapid progression and subsequent
occlusion. The etiology of the stenosis remained unclear,
although the patient did have a positive vascular risk
profile. However, her young age, the dynamic progression,
and the absence of extracranial atherosclerosis argued
against an intracranial atherosclerotic origin. Other vasculopathies were considered but diagnostic tests for these
were negative. Moyamoya disease was considered but
seemed unlikely because of the ICA-sparing pattern and
of the progression of the disease (for further discussion on
moyamoya disease, see also Case 9, p. 171).
The rapid progression of vessel narrowing, recurrent
ischemia despite medical treatment, and the impaired
cerebrovascular reactivity (CVR) diagnosed by acetazolamide xenon-CT led to the decision to perform an EC–IC
bypass operation. This intervention, introduced in 1967,
however, has been the subject of controversy since the
EC–IC Bypass Study was published in 1985. This study
demonstrated that EC–IC bypass operation in patients
with symptomatic high-grade ICA, high-grade MCA stenosis or occlusion did not yield better results than the best
medical treatment (TheEC/IC Bypass Study Group 1985). A
total of 1377 patients were included into this trial, of
whom 714 were treated medically and 663 surgically.
The technical results of the surgical interventions were
good as 96 % of all bypasses remained patent. The dominant vascular pathology in the surgical group was extracranial ICA occlusion in 58.1 %, of whom 64 % were asymptomatic since the first event. The remaining patients had
presented with recurrent cerebrovascular events. A distal
extracranial ICA stenosis was present in 15.4 %, and 14.4 %
hadMCAstenosisand12.1%MCAocclusion.Theobserved
30-day surgical mortality and major stroke morbidity rate
was 0.6 % and 2.5 %, respectively.Fatal and nonfatal strokes
occurred significantly more times and earlier in the surgery group. When perioperative strokes were included,
surgery led to a 14% increase in relative risk of fatal and
nonfatal stroke. In particular, patients with recurrent ischemic events and MCA stenosis revealed less favorable
clinical outcomes. Functional outcome comparison between both groups after a mean observation period of
3.5 and 3.8 years, however, was similar. Subsequently,
EC–IC bypass surgery was largely abandoned and only a
few specialized centers still have the expertise to perform
this type of operation.
In a recent study of 65 heterogeneous patients with 71
EC–IC bypass insertions, no postoperative strokes or
deaths were reported (Tummala et al. 2003). A second
studyof67patientswith73STeA-MCAbypassesinsymptomatic ICA occlusion reported a periprocedural morbidity
rate of 3 % and no mortality. Despite a 90% bypass patency,
Discussion
Fig. B25.19 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patientin Case 25. Right M1-MCA occlusion
and left M1-MCA stenosis (circles). Collateralization of the right MCA
territory via leptomeningeal collaterals from the right ACA and right
PCA (red arrows). Note the right fetal-type PCA.
11 % of cases experienced afurther ischemic eventduring a
mean follow-up of 44 months. (Mendelowitsch et al.
2004).
Known postoperative complications other than isch-
emia are subdural hygroma and hematoma, epidural hematoma, seizures, and meningitis. In our case, a subdural
hematoma occurred during the postoperative course and
required a second surgical intervention. Apart from the
above complications, other unwanted events may occur
which donot necessarily increase the morbidity. Theseare,
for example, a secondary bypass occlusion, occurring in
approximately 5–10% of cases, or a secondary MCA occlusion in cases where high-grade MCA stenosis had been the
indication for the bypass operation. Our patient had both
complications. Although the underlying reason is unclear,
the bypass occlusion may have been facilitated by the
cessation of antiplatelet therapy at the time of surgery
for the subdural hematoma. Considering the MCA occlusion during follow-up two explanations are possible. The
MCA occlusion might have been caused by a bypass-induced reduced perfusion pressure at the site of the stenosis. This mechanism had already been considered to be one
of the reasons for the poor outcome in the MCA stenosis
patients of the EC-IC bypass study. Alternatively, in our
case the MCA occlusion might also have been the natural
course of the primary vascular disease.
Looking at the EC-IC bypass trial from today’s perspec-
tive, the study recruited a rather unselected patient pop-
303
Degree of Neurosonologic Difficulty: High
Case 25 Progressive M1 Middle Cerebral Artery Occlusion
304
ulation, including patients with intracranial ICA and MCA
stenoses and occlusions as well as patients with extracranial ICA occlusions, most of them probably with already
well-established collateral pathways. Considering the high
rate of monosymptomatic patients with ICA occlusion the
latter might even have been the main group of recruited
patients who would have then of course have better outcomes without additional peri-interventional risks. CVR
was not tested in any of the trial patients. An impaired
CVR, however, results in an increase in the risk of stroke
recurrence. In an analysis of 20 follow-up studies of
patients with transient ischemic attacks (TIAs) or minor
ischemic stroke associated with an occluded ICA, patients
Degree of Neurosonologic Difficulty: High
with reduced CVR had an annual ipsilateral stroke risk of
9.5 % compared with 2.1% in all symptomatic patients. In
exhausted CVR, the ipsilateral annual stroke rate was 31 %
(Klijn et al.1997). An EC–IC bypass can improve or normalize an altered CVR (Anderson et al. 1992, Baron et al. 1981,
Gibbs et al. 1987, Hirai et al. 2005, Schmiedek et al. 1994).
Also, an improvement of previously diminished cerebral
blood flow (CBF) can be achieved. Following bypass surgery a reduced CBF of 595 ± 89 mL/min increased significantly by 78 ± 43 mL/min measured with phase-contrast
MRI (Neff et al. 2004).
The main remaining issue, however, is whether a bypass
subsequently reduces stroke recurrence in a high-risk subpopulation. Gathering this information is increasingly difficult as only few specialized centers still have the expertise to perform this type of operation. Currently the North
American Carotid Occlusion Surgery Study (COSS) is recruiting patients with symptomatic ICA occlusion and ipsilateral increased cerebral oxygen extraction fraction
measured by positron emission tomography (PET) instead
of impaired CVR to analyze the potential clinical benefit
from an STeA–MCA bypass. In this large randomized trial,
372 patients will be randomized (Grubb et al. 2003). Hopefully, results of this study will help to ascertain its significance, and if so, to identify those patients who will benefit
from bypass surgery.
Angiologic and Anatomic Aspects
The initial ultrasound findingintheright-sidedM1-MCA
segment was interpreted as a near occlusion. This was
based on the coexistence of a long-segmented M1-MCA
color-mode signal and the low flow pattern with a flow
velocity of 17/10 cm/s. In contrast with the well-defined
near occlusions in the extracranial ICA, there are no clear
recommendations regarding the intracranial circulation.
Similar to the flow dynamics in extracranial ICA it can be
assumed that flow velocity increases up to a stenosis of
> 90 % only. A further increase will then led to a breakdown
of perfusion pressure, subsequent reduction of flow velocity, and finally result in vessel occlusion. Reduced flow
velocities may, according to the physics of flow, also be
found in long-segmented stenoses of a lesser degree. This
might be an alternative explanation of the TCCS finding in
our patient (for further discussion on MCA near occlusion,
see also Case 30, p. 338, and discussion on extracranial ICA
near occlusion, see also Case 15, p. 215).
The evaluation of the contralateral, clinically symptomatic, left-sided M1-MCA segment by different techniques
yielded ambiguous results. Ultrasound analysis demonstrated a mild turbulence and a mildly raised nonanglecorrected flow velocity of 183/83cm/s interpreted as a
low-grade stenosis, which could not be confirmed by
DSA. On follow-up TCCS again, low-grade M1-MCA stenosis was diagnosed and was then further supported by TOF
MRA findings. M1-MCA systolic flow velocities between
155cm/s and 220cm/s have been reported to correlate
well with stenoses < 50 % diagnosed by DSA comprising a
sensitivity,specificity,and positive and negative predictive
values of 94 %, 100 %, 95 %, and 100 %, respectively (Baumgartner et al.1999). The mean value of M1-MCA stenosis in
thisstudymeasuredbyDSAwas36.8%.Thequestion
therefore arises whether DSA is sensitive enough to detect
low-grade intracranial stenoses in all instances. As a mild
stenosis might be eccentric in location, it might not be
appropriately visualized in standard posteroanterior and
lateral projections. Ultrasound and time-of-flight (TOF)
MRA are both flow-sensitive methods. Ultrasound flow
velocities are directly related to the square of the vessel
diameter and are therefore particularly sensitive for lowgrade stenoses. TOF MRA regularly overrates the grade of
stenosis and therefore cannot be used for stenosis graduation, however it will be helpful as a screening method. Its
major limitation is rather to distinguish a real low-grade
stenosis from the frequently observed artifacts suggesting
vessel narrowing. Comparing TCD, TOF MRA, and DSA the
highest correlation was seen in TCD and MRA when analyzing MCA stenoses (Röther et al. 1994). Six stenoses
diagnosed by TCD and MRA were not demonstrated by
DSA in this study. It seems therefore that there is a risk of
overlooking low-grade MCA stenoses with routine DSA,
especially in standard biplanar imaging.
During follow-up, our patient developed a total M1MCA occlusion, demonstrated by the absent arterial signal.
Differentiating near occlusion might be difficult but in our
case occlusion was beyond doubt. The skull bone defects
resulting from the bypass operation yielded optimal transtemporal insonation conditions, permitting an excellent
view of the lateral fissure where the main stem of the MCA
is located. Instead of the MCA, only a low flow signal away
fromtheprobeandattributabletothedeepmiddlecerebral vein was detected. Visualization of accompanying
veins in cases of absent arterial flow signals may also be
used in other locations as a diagnostic aid to confirm
occlusion, for example, the vertebral vein may be visible
in extracranial VA occlusion and the basal vein of Rosenthal in cases of intracranial PCA occlusion.
Main stemMCA occlusions may lead to flow reduction in
the extracranial ICA in the form of a reduced flow velocity
and mild increased pulsatility. This was not the case in our
patient because of the presence of an ipsilateral fetal-type
Discussion
305
PCA. In this constellation the ICAsupplies the ACAand PCA,
both also working as collateral vessels supplying the MCA
territory, which explains why the flow signal of the extracranial ICAwas not altered. As a fetal-type PCA is present in
about 10 % of subjects, such a constellation can be regarded
as an exception. In most cases, reduced flow velocity and
mildly increased pulsatility in the extracranial ICA ishighly
indicative of a distal obstruction of the proximal MCA or
distal ICA (for further reading see also chapter 5, “Intracranial Anterior Circulation,” p. 96 and Ta b l e A 5 . 4). In our
patient, TCCS was not able to visualize the PCoA directly.
Because of the normal flow pattern of the extracranial ICA,
however, a prominent PCoA was assumed to be present,
which was later confirmed by DSA. In case of doubt, the
oscillation test can be used to verify a fetal-type PCA (for
further details about the oscillation test, see also Chapter 2,
“Intracranial Arteries,” p. 24).
Finally, ultrasound bypass evaluation should be discussed. At first we recommend palpating gently the proximal STeA and follow the vessel course toward the trepanation defect. Using TCCS, the main stem of the STeA and
the bypass then can be insonated directly. In patients with
extracranial ICA occlusion and a well-functioning bypass,
the M2-MCA branches and even the M1-MCA segment
itself may show a retrograde flow. On short STeA compression, flow decreases or even completely ceases. A less
patent bypass may lead only to partial, peripheral retrograde MCA blood flow while the M1-MCA segment continues to have compromised orthograde flow (Umemura
etal.2002).Awell-operatingbypasscanalsoberecog-
nized by a raised flow velocity and reduced pulsatility
within the STeA (Arakawa et al. 2003, Inoue and Fujimoto
2005). Most relevant, however, is the resulting blood volume flow as a direct marker of CBF. The question of how
much blood can be contributed via the bypass is, for example, defined by the size of the donor and recipient vessels
as well as by the degree of the actual hemodynamic impairment. Following these considerations, donor and recipient vesselsshould have a minimal diameter of 1 mm. A
phase-contrast MR imaging study reported volume flow
levels of 84 ±32 mL/min (range 14–177 m L /mi n ) w i t h i n
the analyzed bypasses (Neff et al. 2004). Assuming a
mean volume flow of 150–200 mL/min carried by the
MCA in healthy individuals, a bypass may therefore be
able to provide the necessary volume flow of the total
MCA territory. This goal is probably rarely achieved. However, even a 50 % substitution of the MCA territory blood
flow requirements might be sufficient for clinical stabilization if additional leptomeningeal collateral flow is
present. Ultrasound measurements of STeA blood flow
volume in bypass patients have not yet been reported.
The CTA technique does not permit direct volume flow
measurements but may clearly visualize the integrity and
caliber, as wellas potential stenoses of the bypass (Teksam
et al. 2004) (see also chapter 6, “Angiographic Techniques
in Neuroradiology,” and Fig. A6.11D). In addition, CT perfusion may be performed in order to assess the parenchymal perfusion status as the primary therapeutic target of
bypass surgery.
Degree of Neurosonologic Difficulty: High