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Case 4 Temporal Arteriovenous Malformation
146
Degree of Neurosonologic Difficulty: Low
Fig. B4.11 TCCS (transtemporal approach), right-sided insonation,
thalamic plane. Normal flow signal in the right basal vein of Rosenthal (flow velocity: 13/10 cm/s).
Fig. B4.13 DSA, left ICA injection, lateral view. A similar picture is
seen in the lateral view. Note the prominent basal vein of Rosenthal
(arrows).
Fig. B4.12 DSA, left ICA injection, posteroanterior view. Contrast
filling of a vessel convolute mainly via the anterior choroidal artery
(selective angiogram, not shown). Note the prominent basal vein of
Rosenthal surrounding the midbrain (arrows).
Fig. B4.14 DSA, left VA injection, posteroanterior view: Filling of the
AVM via the proximal PCA and its branches. Norelevant opacification
of the distal PCA. Note the prominent basal vein of Rosenthal
(arrows).
Discussion
Clinical Aspects
We have described a patient with symptomatic epilepsy
comprising complex-partialseizures due to a left temporal
AVM in the hippocampal area. Seizures unrelated to hemorrhage are the second most common symptom at initial
presentation in patients with AVM. An analysis of 1289
patients with AVM from three centers found focal seizures
in 9–11 % and generalized seizures in 27–35 % of cases
(Hofmeister et al. 2000). AVMs located near the cortical
surface or within the vascular border zones seem to be
associated with a higher risk of seizures (Stapf et al. 2000).
Intracranial hemorrhage is the most common clinical
presentation and occurs in about 50 % of cases. Depending
on the site of the lesion and its angioarchitecture, the
Discussion
147
hemorrhage can be primarily parenchymatous, subarachnoid, ventricular, or anycombination of these. The need for
treatment strategies is driven by the bleeding risk, which
ranges between 2 % and 4 % per year in patients without
previous hemorrhage (Choi and Mohr 2005). Higher annual rates of up to 18 % per year have been reported in
patients who initially present with a hemorrhage (Arteriovenous Malformation Study Group 1999). The subsequent
bleeding risk is highest in the first year after the initial
hemorrhage and declines rapidly. Factors that seem to
further increase the risk of hemorrhage may be primarily
structural (e. g., the presence of a deep venous drainage, a
deep periventricular location, an aneurysm), and may also
be dynamic (e. g., the presence of a high feeding artery
pressure or a slow arterial filling) (Duong et al.1998, Fleetwood and Steinberg 2002). Dynamic aspects in particular,
such as the flow velocity of arterial feeders, have been
associated with an increased risk of intra- and postoperative neurosurgical treatment complications (Pasqualin et
al. 1991). Furthermore, a history of hypertension, young
age, and male gender has been associated with an increased risk whereas an AVM located in the arterial borderzone seems to result in a lower risk of bleeding (Mast et
al. 1997, Stapf et al. 2000). Looking at correlations between
lesion size and bleeding risk, the results are contradictory,
ranging from a positive association to irrelevant.
Headache is the presenting symptom in 10–19 % of p atients with AVM (Hofmeister et al. 2000). There are no
pathognomonic characteristics of headache associated
with intracranial bleeding. In particular, there are no safe
criteria to differentiate symptomatic from primary headaches such as migraine. However, the incidence of AVMs is
not higher within the group of migraine patients (Evans
1996).
Patients may present focal neurologic signs even in the
absence of underlying hemorrhage. The reported rates of
such deficits varies widely between 1 % and 40 %, depending on the definition used. Progressing neurologic deficits
was observed in about 4–8 % of patients. As a potential
underlying mechanism, a “steal phenomenon” caused by
hypoperfusion and subsequent ischemia in the brain tissue
surrounding the AVM has been postulated, but this hypothesis has been criticized by others (Mast et al. 1995a).
Treatment decisions for patients with AVMs in the brain
should include a comparison of the risks of the natural
course of the condition with the interventional periprocedural risk of each therapeutic approach (Al-Shahi and
Warlow 2001). Treatment is a growing interdisciplinary
challenge and should be focused on prevention and resolution of hemorrhage. The available treatment options are
open surgery,radiotherapy, and endovascular therapy, and
the latter is currently the most frequently used technique.
If possible, total surgical resection of the AVM should be
performed, preferably during one operation; this is the
best-known treatment. Endovascular embolization which
reduces the size of the malformation can reduce the risk of
hemorrhage before surgery or radiotherapy but frequently
fails to completely obliterate the AVM. Stereotactic radiosurgery causes subsequently sclerosis of the blood vessels,
obliterating the AVM over a period of 1–2years.Theadvantage of the latter method is the opportunity to treat
patients with deep-seated AVMs or in eloquent brain regions, which carries a high risk of complications in open
surgery. Its major limitation is the treatable size of the
AVM. Best results are achieved if the AVM nidus measures
less than 2 cm.
There is scarce objective information about the efficacy
and outcome of treatment, reflecting a lack of long-term
follow-up and inconsistencies in treatment evaluation.
ThereportedrateofobliterationofAVMsaftersurgery
confirmed by angiography is up to 97 % (Castel and Kantor
2001). Endovascular embolization of the AVM alone is
estimated to be successful in 13–40% of patients (Hartmann et al. 2002). Total obliteration by stereotactic radiosurgery is successful in up to 24 % of cases (Maruyamaet al.
2005). Therefore, a multimodal treatment strategy combining the above approaches has evolved within the past
two decades.
However, there is also growing awareness that treatment to prevent intracranial bleeding itself carries risks
of disabling or fatal outcome and untreated AVMs may
have a good prognosis, so thatthe benefit and risks should
always be assessed in each individual patient. Grading
according to the Martin–Spetzler scale is the most frequently used method to classify AVMs and to evaluate
the risk of surgical resection (Spetzler and Martin 1986).
The scale includes factors such as AVM size: < 3 cm (1), 36 cm (2) or > 6 cm (3 points), the type of venous drainage:
superficial only (0) or deep (1 point), and the location of
the AVM: non-eloquent (0) or eloquent (1 point). Increased surgical risk is associated with higher AVM grade
which is calculated by awarded points.
In our case, surgical resection was considered to have a
high risk because of the eloquent localization (1) of the
AVM, a size of about 3 cm (2), and the deep venous drainage (1 point) resulting in a Martin–Spetzler grade IV. Radiosurgery was not indicated because of the large size of
the AVM. Partial endovascular embolization was considered to be a viable treatment option, however our patient
decided against therapy. The clinical course over 4 years so
far and the effective anticonvulsive management seems to
support the use of purely symptomatic treatment in this
case.
Angiologic and Anatomic Aspects
AVMs are thought to be caused by errors during development during the embryonic or fetal stage of vessel formation. The low prevalence in infants suggests that the development of AVMs may extend over decades. The basic
pathology of an AVM is the direct connection of arteries
and veins bypassing the capillary bed, subsequently leading to dilatation and a tortuous course of the affected veins.
The histopathologic differentiation of the arterial and ve-
Degree of Neurosonologic Difficulty: Low
Case 4 Temporal Arteriovenous Malformation
148
nous proportion of the AVM is difficult, as the affected
vessels frequently demonstrate a thin or deficient tunica
media and internal elastic lamina. AVMs are more frequently found in a supratentorial location; there are no
other sites of predilection. The typical AVM angioarchitectureiswedgeshaped,withthebasetowardthecerebral
cortex and the apex extending into the brain. Other variants completely lie within the white matter. AVMs that
extend into deep brain structures are generally fed by the
lenticulostriatal, choroidal, or thalamostriatal arteries and
their veins frequently drain into the deep venous system.
The latter AVM variant corresponds to the lesion found in
Degree of Neurosonologic Difficulty: Low
our patient with blood supply via the anterior and posterior choroidal artery and drainage through the left basal
vein of Rosenthal.
CT and MRI have a substantial role in the diagnosis of
AVMs. Location, size, and relation to surrounding intracranial structures can be identified with MR technology.
Furthermore, presence of hemosiderin indicates previous
hemorrhage. DSA remains the gold standard for assessing
the often complex AVM angioarchitecture. The predominance of various feeding vessels and the different vascular
territories involved, potentially present aneurysms as well
as the venous drainage pattern are all evaluated by this
technique and indispensable for treatment planning. New
developments in dynamic CT and MRI techniques increasingly enable the analysis of not only morphologic but also
functional aspects of cerebral perfusion in AVM patients
(for further details, see Case 27, p. 312).
Ultrasound is a noninvasive screening tool for both detection and follow-up evaluation of brain AVMs. While
transcranial Doppler (TCD) only allows assessment of hemodynamic parameters like high flow velocities and low
pulsatility, transcranial color-coded sonography (TCCS)
may furthermore depict the AVM nidus itself, the hemodynamic features of the feeders, and the draining vessels,
which make TCCS more sensitive than TCD. Success rates
in AVM nidus visualization depend more on location than
size. In an analysis of 54 patients with proven AVM on DSA,
a nidus was identified in 72 % of cases. Three further AVMs
were found by detection of feeder flow signals only. The
calculated sensitivity reached 88.9 % for the detection of
AVMs located in the basal aspects of the frontal, parietal,
and temporal lobes, i. e., the regions that can be well
accessed by TCCS if the common examination planes are
used. The smallest detectable nidus diameter reported was
1.5 cm (Bartels 2005). AVMs near the cortical–subcortical
junction of the parietal, frontal, and occipital lobes as well
as the cerebellum are more difficult to detect with TCCS,
even the larger ones.
Using the systolic flow velocity as the diagnostic criterion alone, a prospective study in 114 patients revealed a
sensitivity of 97 % in detecting AVMs > 5 cm and a sensitivity of 84 % in detecting AVMs between 2.6 cm and 5 cm.
Among the small AVMs < 2.5 cm, the AVM was missed in
61 %. Flow velocity correlated with the AVM size, probably
reflecting its volume flow. Lower sensitivitieswere found if
the PI was used as the diagnostic criterion (Mast et al.
1995b).The diagnostic accuracy may be increased by using
echo-contrast agents as shown in a small TCD study in 12
AVM patients, which reported a sensitivity of 92 % (Uggowitzer et al. 1999). Furthermore, a diminished carbon dioxide cerebrovascular reactivity (CVR) can be detected by
TCD, which may be even more sensitive than increased
flow velocities (Diehl et al. 1994).
A recently reported additional ultrasonographic parameter is the global cerebral circulation time. Shortening of
blood passage via arteriovenous shunting in untreated
patients is well known from catheter angiography and
dynamic CT studies (Bartolini et al. 1992, Gilroy et al.
1963). Global cerebral circulation time measures the
time difference between the arrival of a bolus of contrast
between the extracranial ICA and the internal jugular vein
(IJV), using Doppler or duplex ultrasound. Patients with a
high-flow AVM were shown to have a significantly shorter
global cerebral circulation time (3 ±1. 3 s) than h ealthy
controls (7 ±1.3s) (Schreiber et al. 2002, Schreiber et al.
2003b). Global cerebral circulation time did not correlate
with AVM size. As an indirect approach the technique may
even be more sensitive in detecting an AVM than the
assessment of flow velocity and PI, as it will also work in
AVMs in cortical/subcortical locations that are not directly
accessible by TCCS. The test proved to be even more sensitive if applied to occipital dural fistulas, revealing a mean
global cerebral circulation time of 1.1± 0.9 s (Schreiber et
al.2004).Apartfromitsdiagnosticimplication,thistest
has the potential to be used as an additional monitoring
tool for treatment procedures such as stepwise embolization or surgical occlusion. Its clinical relevance has yet to
be evaluated (for further details about global cerebral
circulation time and multimodal ultrasound, see also
Chapter 3, “Parameters of Cerebral Hemodynamics,” p. 60
and Case 27, p. 312).
Improved surgical and endovascular treatment options
have drawn increasing attention toward the cerebral hemodynamic status of patients with AVMs, particularly
aiming to assess the subsequent risk of bleeding. TCCS as
well as TCD are useful applications to analyze flow velocity,
pulsatility, CVR and the global cerebral circulation time.
However, non of these parameters seem to directly correlate with the bleeding risk.
Case 5
M1 Middle Cerebral Artery Stenosis
149
Clinical Presentation
A 48-year-old woman presented with a sudden onset of a
mild left-sided sensorimotor hemisyndrome. A similar
transient event with complete remission had occurred 1
week prior to presentation. The patient had multiple vascular risk factors including arterial hypertension, diabetes
mellitus, hypercholesterolemia, and obesity (National InstituteofHealthStrokeScale[NIHSS]score3).
Initial Neuroradiologic Findings
Magnetic resonance imaging (MRI) of the brain revealed
an ischemic lesion in the frontoparietal region of the right
hemisphere, predominantly in the sensorimotor cortex,
consistent with a partial subacute territorial middle cerebral artery (MCA) infarction. Intracranial time-of-flight
(TOF) magnetic resonance angiography (MRA) showed
an isolated high-grade MCA stenosis of the right M1MCA segment and a hypoplastic left vertebral artery (VA)
(Figs. B5.1, B5.2, B5.3).
Suspected Diagnosis
Recurrent ischemia in the right MCA territory caused by
MCA stenosis of the M1-MCA segment.
Questions to Answer by Ultrasound Techniques
• Were there atherosclerotic vascular changes in the extracranial vessels?
• What was the degree of the stenosis?
• Was there evidence of further intracranial stenotic pro-
cesses, underrated by MRA?
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode imaging revealed no atherosclerotic vascular
changes. Doppler spectrum analysis showed normal and
symmetric flow signals.
Transcranial Duplex Sonography
Doppler spectrum analysis revealed an increased flow
velocity reaching 320 cm/s peak systolic flow in the right
proximal M1-MCA segment at a depth of 58 mm. A mild
poststenotic flow pattern was detected in one right-sided
M2-MCA branch. In comparison withthe left side, the right
A1-ACA segment revealed anincreased flowvelocity without turbulence (peak systolic flow right A1-ACA: 136cm/s,
left A1-ACA: 71 cm/s). Posterior circulation and the left
M1-MCA segment showed normal flow signals (Figs. B5.4,
B5.5, B5.6, B5.7).
Conclusion
High-grade MCA stenosis in the right M1-MCA segment of
hemodynamic relevance without evidence of atherosclerotic changes in the extracranial brain-supplying arteries.
Conventional Angiography (Day 2)
Because of the unremarkable extracranial findings, conventional digital subtraction angiography (DSA) was performed. The segmental high-grade narrowing of the proximal right M1-MCA segment was confirmed. The distal
course of the vessel was normal. The contrast filling of
the right-sided distal MCA branches was mildly delayed
in comparison with the distal branches of the ipsilateral
anterior cerebral artery (ACA). Late arterial phase images
showed mild leptomeningeal collateralization via the ACA.
The left anterior and the posterior circulations showed no
abnormalities (Figs. B5.8, B5.9, B5.10).
Clinical Course
We assumed that the etiology of the stenosis was a result
of the patient’s multiple vascular risk factors. However, the
absence of atherosclerotic vessel changes in the remaining
brain-supplying arteries did not match this hypothesis.
Other potential causes such as thrombophilia, vasculitis,
or an autoimmune etiology were ruled out. A normal
transesophageal echocardiogram and a 24-hour electrocardiogram (ECG) made a cardiac embolic source unlikely.
However, due to the young age of the patient and unresolved etiology of the MCA stenosis, oral anticoagulation
with phenprocoumon was started, to be taken for 6
Case 5 M1 Middle Cerebral Artery Stenosis
150
months, followed by antiplatelet treatment with aspirin.
During the patient’s stay in the hospital, the left-sided
hemiparesis improved slightly. Two years after the presenting event the patient sustained a transient ischemic
attack (TIA) with slight paresis, hypesthesia, and hypalgesia of the left arm. Her medication was then changed to
aspirin and dipyridamole. Early neurosonological followupandregularcontrolsovera4-yearperiodshowedidentical findings.
Degree of Neurosonologic Difficulty: Low
Final Diagnosis
Ischemic brain infarction in the right MCA territory by
artery-to-artery embolization caused by a right-sided hemodynamically relevant high-grade M1-MCA stenosis.
Fig. B5.1 MR FLAIR image, axial plane. Hyperintense signals are
depicted in the right sensorimotor cortex, compatible with a territorial MCA ischemia in the territory of the prerolandic and rolandic
arteries of the MCA.
Fig. B5.3 3D TOF MRA, coronal MIP. Absent flow signal in the proximal right M1-MCA, suggesting vessel occlusion (arrow). Because of
the clear visibility of the distal M1-MCA and M2-MCA segments, a
high-grade stenosis was assumed.
Fig. B5.2 MR T2-weighted image, axial plane. Thin slices (3 mm)
permit the detection of a stenosis in the right proximal M1-MCA
as secondary benefit of MRI cross section assessment (arrows).
Fig. B5.4 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Right M1-MCA with intrastenotic flow velocity of
322/202 cm/s (non-angle corrected) in a depth of 58 mm. Note the
turbulent flow pattern.
Discussion
151
Degree of Neurosonologic Difficulty: Low
Fig. B5.5 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Mild poststenotic flow pattern in a right M2-MCA
branch.
Fig. B5.7 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Left A1-ACA from a right transtemporal approach
with normal orthograde flow (flow velocity: 71/46 cm/s).
Fig. B5.6 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Raised flow velocities in the right A1-ACA (136/
72 cm/s) without turbulence, indicating leptomeningeal collateralization of the MCA territor y.
Fig. B5.8 DSA, right ICA injection, posteroanterior view. Severe
segmental narrowing of the proximal MCA (arrow). The contrast
filling of the right-sided distal MCA branches is mildly delayed in
comparison to the distal branches of the ipsilateral ACA.
Discussion
Clinical Aspects
We have described a 48-year-old patient with a rightsided high-grade M1-MCA stenosis with subsequent cortical ischemic brain infarction in the MCA territory. Because
of the young age of the patient, an embolism from an
extracranial source with secondary partial recanalization
was initially considered.
Embolism is the most common cause of major cerebral
artery occlusion, mostly occurring in the MCA territory
(Lhermitte et al. 1970). Differentiation between a local
thrombus and embolus in the acute state is often not
possible. A partially resolved thrombus might result in
the finding of a stenosis. Other causes of stenosis are an
atheromatous plaque, a dissection, moyamoya disease,
and postradiation effects. The clinical course and followup investigations usually help to clarify the etiology. In our
patient, the stable clinical and neurosonologic findings
Case 5 M1 Middle Cerebral Artery Stenosis
152
Degree of Neurosonologic Difficulty: Low
Fig. B5.9 DSA, right ICA injection, posteroanterior view. Enlarged
view of the stenotic proximal right M1-MCA.
over several years of follow-up were suggestive of a fixed
MCA stenosis. Although she had multiple vascular risk
factors, assessment of the extracranial brain-supplying
arteries did not demonstrate atherosclerosis. A cardiac
embolic source, thrombophilia, vasculitis, and the present
of an autoimmune disease could not be identified. Finally,
a rare distribution pattern of atherosclerosis comprising an
isolated plaque in the main stem MCA leading to artery-toartery embolism with subsequent infarction was assumed.
Although predominant intracranial atherosclerosis is rare
in Caucasians, it is a well-known finding, for example, in
the Asian stroke population (Suwanwela and Chutinetr
2003).
Atherosclerosis is well recognized as the major cause of
vascular disease in the extracranial brain-supplying arteries. In contrast, little is known about the incidence
and prevalence of intracranial atherosclerotic lesions.
Early autopsy studies indicated that thrombotic MCA occlusions were an uncommon cause of stroke. However, in
the past decade, the literature indicates intracranial atherosclerosis as a common etiology of cerebral ischemia. In
a Caucasian population, intracranial atherosclerosis is
found in approximately 5–10 % of stroke patients (Caplan
et al. 1986, Sacco et al. 1995), whereas it is the most
commoncauseofstrokesintheAsianpopulation.Data
regarding the distribution of intracranial atherosclerosis
are scarce. Conventional angiography in the chronic state
after stroke, independent of the presumed etiology, revealed the basilar artery (8% of cases) as the most frequent
location of atherosclerotic stenoses followed bythe carotid
siphon (6 %), the intracranial VA (5 %), the MCA (4 %), and
finally the ACA and posterior cerebral artery (PCA) (2–3%)
(Hassetal.1968).Akinsandcoworkers(1998)reportedthe
Fig. B5.10 DSA, right ICA injection, posteroanterior view. Late arterial phase demonstrates the mild leptomeningeal collateralization of
the right MCA territory via the right ACA. Lines indicate the borderzone areas.
intracranial ICA as the most frequent site of intracranial
stenosis, accounting for about 50 % of cases. Other authors
assume that 35–40 % of cases involve the intracranial vertebrobasilar vessels (Chimowitz et al. 1995).
Risk factors for intracranial atherosclerosis are similar to
those for extracranial atherosclerosis and coronary artery
disease, and include diabetes, hypertension, smoking, and
hypercholesterolemia, and also non-Caucasian race (Sacco
et al. 1995, Wityk 1996). Little is known about the natural
course of intracranial stenoses. The WASID (Warfarin Aspirin Symptomatic Intracranial Disease) study followed up
569 patients with symptomatic intracranial stenoses
greater than 50 % over a mean period of 1.8 years and
revealed recurrent stroke in 19 %. Of these, 77 % were located within the territory of the stenotic artery. The stroke
risk was substantially increased with stenoses ≥ 70 %, and
the authors also found women to be at greater risk. No
correlation was found with the site of stenosis, with the
initial clinical presentation or with prior use of an antithrombotic medication (Kasner et al. 2006). Similar findings were reported in a smaller prospective multicenter
study of 102 symptomatic patients; 60.7 % had a recurrent
stroke or TIA within the territory of the stenotic artery
during a mean follow-up of 23.4 months if the stenosis
was hemodynamically significant (Mazighi et al. 2006).
Other prospective studies in patients with symptomatic
MCA stenosis reported annual ipsilateral stroke rates ranging from 2.3 % to 9.1 % (Arenillas et al. 2001, Gao et al. 2004,
Kern et al. 2005). Asymptomatic MCA stenoses instead
have an annual ipsilateral stroke rate of 0–1.4 % , wh i c h is
comparable to that in asymptomatic extracranial carotid
artery disease (Kremer et al. 2004, Kern et al. 2005, Hennerici et al. 1987).
Discussion
153
Data about the evolution of vessel pathology over time
are scarce. Both progression and regression have been
reported in intracranial atherosclerosis, the latter probably
being attributed to resolution of intravascular thrombi
(Akins et al. 1998). Progression of intracranial atherosclerosis has been positively correlated with further vascular
events (Arenillas et al. 2001). Also, the presence of microembolic signals assessed by transcranial Doppler (TCD) has
been shown to independently predict the occurrence of
future ischemic events (Gao et al. 2004).
There is ongoing controversy about the best therapeutic
strategies for patients with symptomatic intracranial atherosclerosis. Medical treatment is based mainly on risk
factor management. The primary aim is to control hypertension, diabetes, and hypercholesterolemia and to stop
smoking. Although these patients have a high risk of recurrent stroke no prospective studies have compared antithrombotic treatments. Suggested treatment strategies
so far include various combinations of aspirin, statins,
ticlopidine, clopidogrel, and warfarin. In 1995, the retrospective WASID trial demonstrated an annual recurrent
stroke rate of 3.6% and 10.4% in the patient group treated
with warfarin and the aspirin group, respectively (Chimowitz et al. 1995). On the basis of these results, a prospective
randomized trial was started in symptomatic patients, but
this study could not prove superiority of anticoagulation.
Instead, enrollment of patients was stopped because of
adverse effects of warfarin. During a mean follow-up of
1.8 years, death and major hemorrhage was significantly
higher in the warfarin group than in the aspirin group
(9.7%vs.4.3%and8.3%vs.3.2%,respectively)(Chimowitz
et al. 2005).
Considering the high risk of stroke recurrence despite
the use of antithrombotic treatments, alternative treatment strategies are needed. With the recent technologic
advancements in endoluminal revascularization, intracranial angioplasty and stenting have emerged as promising
alternatives. Early results, however, using balloon expandable coronary stents, were disappointing as morbidity of
up to 20 % was reported. Since then, stents designed particularly for intracranial use have been developed. The
SSYLVIA (Stenting of Symptomatic Atherosclerotic Lesions
in the Vertebral or Intracranial Arteries) study looked at
safety and feasibility of intracranial stents in 61 patients
(43 symptomatic intracranial stenoses ≥ 50 %, five of them
MCA stenoses) and yielded promising results. Successful
stent placement was achieved in 95 % of patients. Strokes
occurred in 6.6 % of patients within 30 days and in 7.3%
between 30 days and 1 year. Re-stenosis was observed in
35 % of patients, and 61 % of them remained asymptomatic
during 1 year of follow-up (SSYLVIA Study Investigators
2004). So far, two further prospective multicenter studies
have reported comparable results using a new developed
self-expanding stent (wingspan) for intracranial stenoses.
In the first study, which included 45 patients, the ipsilateral stroke/death rate was 4.5 % within the first month.
After 6 months the ipsilateral stroke/death rate was 7 %,
and the overall stroke rate and mortality were 9.7 % and
2.3 %, respectively. The mean degree of stenosis before,
immediately after stenting, and at 6 months follow-up
was 75%, 32%, and 28%, respectively (Bose et al. 2007).
The second study, which included 78 patients, reported an
immediate decrease of stenosis from 75 % to 27% after
stenting. The 30-day rate of major periprocedural neurologic complication and death was 6.1% (n= 5). As four of
these patients died, the actual mortality was 5 %. New
ischemic lesions on MR diffusion-weighted imaging were
seen in 34.2 % patients, of which 77 % were asymptomatic
(Fiorella et al. 2007). Periprocedural morbidity andmortality associated with stenting techniques still seem high and
need to reduce further. Future studies should help to identify patient groups at particularly stroke risk, and those
who may benefit from interventional treatment.
Angiologic and Anatomic Aspects
Ultrasound is now widely available, and is one of the
principal noninvasive tools for the evaluation of intracranial occlusive artery disease. In general, intracranial stenoses are characterized using direct and indirect ultrasound
criteria, both of which contribute to the grading of stenoses. Direct signs are locally raised intrastenotic flow velocities and turbulences. Indirect signs are reduced velocities in the altered pre- and/or poststenotic vessels segments, and/or poststenotic flow patterns as well as raised
velocities in collateral vessels (for further information, see
also Chapter 5 “Stenoses and Occlusions,” p. 81 and “Collateral Pathways,” p.101). Despite the several TCD studies
that have described criteria for the detection of intracranial stenoses, there are no uniform internationally accepted criteria, like for example in extracranial carotid
artery stenosis (de Bray et al. 1988, Felberg et al. 2002,
Ley-Pozo et al. 1990, Mattle et al. 1988, Röther et al. 1994).
Comparing TCD with TOF MRA and DSA sensitivity, specificity, and positive and negative predictive values of 94 %,
91 %, 78 %, and 98 %, respectively, have been reported (Felbergetal.2002).InacutestrokeTCDrevealedasensitivity
and specificity of 79 % and 94 % compared with computed
tomograph angiography (CTA) in an analysis of 132 patients (Tsivgoulis et al. 2007). In regard to MCA stenosis of
≥ 50 % using conventional angiography as reference
method a sensitivity of 92 %, specificity of 92 %, positive
predictive value of 88 % and negative predictive value of
98 % for 80 cm/s average maximal velocity cut-off has been
reported when analyzing six reports (Navarro et al. 2007).
Less favorable results were referred in the recently published SONIA (Stroke Outcomes and Neuroimaging of Intracranial Atherosclerosis) trial. The study included 407
patients from the WASID trial and compared the accuracy
of TCD and MRA to diagnose an intracranial stenosis > 50 %
compared with DSA. For TCD, > 50% stenosis was defined
as an average maximum velocity: > 100 cm/s for the MCA;
> 90 cm/s for the ICA; and > 80 cm/s for the basilar artery
and VA. The MRA criteria were a lumen reduction more
Degree of Neurosonologic Difficulty: Low
Case 5 M1 Middle Cerebral Artery Stenosis
154
than 50 % or the presence of a flow gap. Applying these
criteria, positive and negative predictive values on TCD
were 36 % and 86 % and on MRA were 59 % and 91 %, respectively.It was concluded that TCD and MRA can exclude
but not confirm reliable a stenosis > 50 % (Feldman et al.
2007).
Accurate vessel identification may be a major concern in
TCD. TCCS overcomes these shortcomings, ensuring unequivocal vessel identification in most cases. One relevant
study comparing TCCS and DSA reported data on peak
systolic velocity values. For MCA main stem stenosis,
flow velocities of ≥ 220 cm/s and ≥ 155 cm/s were reported
Degree of Neurosonologic Difficulty: Low
to ensure the definite presence of a ≥ 50 % or < 50 % stenosis
with a sensitivity, specificity, and positive and negative
predictive values of 100 % for ≥ 50 % stenosis, and 94 %,
100%,95%,and100%,respectively,for<50%stenosis
(Baumgartner et al. 1999). Angle-correction was performed if a straight vessel segment of about 2 cm was
present. However, care should be taken when interpreting
raised flow velocitiesas intracranialstenoses. Other causes
of flow velocity increase may be the presence of a vascular
malformation and hyperemia, caused for example by head
trauma or subarachnoid hemorrhage (SAH). A circumscribed, focal velocity increase may help to differentiate
these pathologies.
In our case, a markedly increased localized intrastenotic
M1-MCA systolic flow velocity of 320 cm/s, a mild poststenotic flow pattern distal of the stenosis, and the mild
activation of leptomeningeal collateral pathways via a
raised ipsilateral A1-ACA flow facilitated the diagnosis of
a hemodynamically relevant high-grade MCA stenosis of
at least about 80 %.
What is the role of the other available methods in eval-
uation and grading of intracranial stenoses? For decades,
DSA has been the only method for direct imaging of the
intracranial circulation. But until recently, no special grading system has been developed and stenoses were usually
estimated by “eyeballing.” DSA also had technical shortcomings as it is commonly performed in two standard
levels of projection (posteroanterior and lateral). However,
for MCA evaluation, the lateral image does not allow suffi-
cient evaluation of either the distal or proximal segments.
In presumed mild to moderate stenosis, oblique and rotated views would be required, but these views are not
part of the routine diagnostic algorithm in a presumed
stenosis. This may be one explanation for the “false-positive” MCA stenoses found in TCD compared with DSA
resulting in a low positive predictive value of only 36 % in
the SONIA trial (Feldman et al. 2007). The second reason is
the particular sensitivity of ultrasound within the range of
mild to moderate stenoses as flow velocity is inversely
relatedtothesquaredvesseldiameter.Exactquantification of low-grade stenoses by DSA is difficult, not at least
because of the small vessel diameters of 2–3mm in their
main stems.
The systematic approach of using DSA for graduation of
stenoses ≥ 50%wasfirstadoptedintheWASIDstudy.The
stenoses were graded by using the residual and the assumed normal vessel diameters. The latter was measured
proximal tothe stenosis within the widest visible segment.
If this was not available, the next normal distal segment
was used. If the complete M1-MCA or basilar artery (BA)
was affected, the distal ICA or the dominant intracranial VA
was used. For all intracranial ICA stenoses, the petrosal ICA
segment, or if also involved, the most distal extracranial
ICA diameter, were used as the reference. A 99 % stenosis
was diagnosed if a “gap sign,” defined as an absent vessel
signal over a short distance, was observed. In an analysis of
24 affected intracranial arteries, the interobserver agreements for the three participating readers ranged from 71 %
to 100 % and the intraobserver agreements ranged from
83%to100%(Samuelsetal.2000).However,onlyconventional lateral and postero-anterior images were used and
patients were only included if a lumen reduction greater
than 50 % was found on “eye ball” examination, so that
low-grade stenoses were not studied.
In recent years, DSA has lost diagnostic importance because of the risk of periprocedural stroke and the competing noninvasive or less invasive diagnostic options—MRA
and computed tomograph angiography (CTA). Depending
on the applied technique, a number of potential pitfalls
have to be considered. MRA, usually performed as a noncontrast TOF technique is a fast acquisition technique
which is, however, flow dependent. High flow velocities
or turbulent flow lead to a loss of signal which may be
difficult to interpret. Our patient had MRA signal reduction
in both carotid siphons as well as in the proximal M1-MCA
segment, the former being caused by the physiologically
turbulent flow within the carotid siphon and the latter
being due to vessel stenosis. Furthermore, TOF MRA tends
to overestimate the degree of stenosis. A short signal gap
with preserved distal vessel segments—as in our patient—is not an occlusion but corresponds with a highgrade stenosis. In real occlusion, there is usually a long
signal gap with obviously reduced distal vessel segments
or total absence of signal. In the SONIA trial a low positive
predictive value of 59 % has been reported (Feldman et al.
2007). Increased field strength and parallel imaging techniques in MRA improve detail resolution, although inherent limitations such as flow dependency persist. In unclear
cases it may be helpful to analyze the source images as the
sensitivity of these will increase (Korogi et al. 1997).
Although unconventional, even the assessment of flow
voids on normal axial T2 weighted images may contribute
to the evaluation of vessel patency, demonstrated in our
case in Figure B5.2.
Multislice CTA is the most recent technique and provides
excellent intracranial spatial resolution and fast data acquisition times but involves x-ray exposure and contrast
injection to the patient. Comparison of CTA and TOF MRA
for the detection of intracranial stenoses with DSA as
reference method revealed a higher sensitivity (98 % vs.
70 %) and a higher positive predictive value (93 % vs. 65 %)
for the CTA technique. At least in selected constellations of
Discussion
155
distal BA near occlusion CTA was even superior compared
with DSA, where DSA due to low flow phenomena or
retrograde BA flow suggested total BA occlusion (Bash et
al. 2005). A combination of CTA and MRA may yield a
diagnostic accuracy similar to DSA (Hirai et al. 2002).
In the near future, new MRI protocols, contrast-en-
hanced MRA, and advanced multislice CT scanners will
be available and facilitate detection and graduation of
intracranial stenoses. Of particular interest will be techniques applicable in hyperacute stroke for the assessment
of all the intra- and extracranial brain-supplying arteries
and also for follow-up examinations. Modern ultrasound
methods, especially TCCS, will therefore not only compete
with, but also complete, modern MRA and CTA imaging.
Degree of Neurosonologic Difficulty: Low