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439Discussion
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Visualization of an unaff ected PCoA, however, is a
major concern for ultrasound methods also. In healthy
young subjects TCCS fails to directly visualize the PCoA
in up to 35% of cases (Klötzsch et al 1996b) and in elderly patients it fails in up to 85% of cases (Hoksbergen
et al 2000a). The low detection rate is mainly explained
by the low fl ow state in an unaff ected PCoA, its small
size, the unfavorable angle of insonation which might
reach 90°, and the vessel course, which often does not
run straight between anterior and posterior circulation.
Especially in elderly patients, an elongated vessel course
can be frequently observed, leading to equivocal or bidirectional fl ow patterns (for further discussion on col-
lateral vessels, see also Chapter 5, “Primary Collaterals
(ACoA and P CoA)” u nder “ Int racran ial Coll ater al Pathways in ICA Occlusive Processes”).
440
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Case 31
Dissection of the Right Internal Carotid Artery C6 Segment
Clinical Presentation
A 46-year-old woman was admitted with slight numbness and weakness in the left hand which began 5 days
before presentation. At fi rst, she felt only mildly aff ect-
ed and refused to seek medical attention. The day before
symptom onset, she had suff ered unusually severe right-
sided headaches. She reported no trigger events and had
no previous medical problems. She had no known vascular risk factors and, in particular, no history of migraine.
Neurologic examination revealed a mild sensorimotor
paresis of the left hand and reduced fi ne motor skills (Na-
tional Institute of Health Stroke Scale [NIHSS] score: 2).
Initial Neuroradiologic Findings
Initial CT showed normal fi ndings (not shown).
Suspected Diagnosis
Right-sided middle cerebral artery (MCA) ischemia in
internal carotid artery (ICA) dissection.
Questions to Answer by Ultrasound
Techniques
• Is there a steno-occlusive lesion in the right anterior
circulation?
• Are there signs of ICA dissection?
compared with 74/35 cm/s on the left side. Transforaminal examination of the VAs was normal (Fig. B31.1 and
Fig. B31.2). No microembolic signals were detected during routine transcranial color-coded duplex sonography
(TCCS) examination.
Follow-up Neuroradiologic Findings
(Day 2)
Assuming a right-sided MCA ischemia caused by a right
C6-ICA stenosis, MRI including time-of-fl ight angiog-
raphy (TOF-MRA) was performed on the same day. MRI
diff usion-weighted images revealed hyperintense sig-
nals in the right MCA territory, including the region of
the hand knob (omega region). TOF-MRA showed a right
C6-ICA tailoring and a hyperintense structure below the
C6-ICA indicative of blood extravasation. Fat-suppressed
T1-weighted images displayed a crescent-shaped wall
hematoma. The right-sided A1-ACA segment and the
right posterior communicating artery (PCoA) were not
visible (Fig. B31.3, Fig. B31.4, Fig. B31.5).
Conclusion
Fragmented right-sided MCA infarction due to artery-toartery embolism arising from C6-ICA stenosis caused by
circumscribed spontaneous dissection.
Fig. B31.6 shows a schematic of the patient’s extra-
and intracranial brain-supplying arteries.
Initial Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
Examination of the carotid and vertebral arteries (VAs)
revealed normal results. No direct or indirect signs of a
cervical artery dissection (CAD) were observed.
Clinical Course (1)
Anticoagulation was considered but not initiated. We decided against anticoagulation to avoid increasing the risk
of secondary ICA occlusion at the dissection site, given
the special anatomic cerebral arterial circle (circle of Willis) constellation and lack of collateral pathways on the
right side. Therefore, secondary prevention with aspirin
was started.
Transcranial Duplex Sonography
Normal fl ow signals were found in both M1-MCA and
the detectable M2 segments as well as in the anterior
(ACA) and posterior (PCA) cerebral arteries. The carotid siphon and carotid-T showed normal fl ow signals
on both sides. An apparent diff erence was seen in the
C6-ICA segment. The right ICA showed increased and
nonturbulent fl ow with a fl ow velocity of 121/46 cm/s
Follow-up Neurosonologic Findings
(Day 120)
Transcranial Duplex Sonography
Normal fl ow parameters were found in all vessel seg-
ments including the right C6-ICA (not shown).
441Follow-up Neurosonologic Findings (Day 120)
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
C6-ICA-R
Fig. B31.1 TCCS (t rans tempo ral approach) , right -sid ed in sona tion,
lower pontine plane. Non-angle-corrected increased but nonturbulent fl ow in the right C6-ICA (fl ow velocity 121/46 cm/s).
AB
C6-ICA-L
Fig. B31.2 TCCS (tr anst emporal appro ach) , left -sided insonati on,
lower pontine plane. Normal (and lower) fl ow velocities on the un-
aff ected left C6-ICA (fl ow velocity 74/35 cm/s).
AB
Fig. B31.3 (A,B) MRI, diff usion-weighted image, axial plane. Hyper-
intense signals in the right MCA territory (arrowhead) representing
acute multiple small infarctions including the hand knob (arrow).
AB
Fig. B31.5 MRI, T1-weighted fat-suppressed images, sagittal
plane. (A) A crescent-shaped intramural hematoma leading to a
l u m e n r e d u c t i o n o f ~ 6 0 % c a n b e s e e n i n t h e r i g h t C 6 - I C A ( a r r o w ) .
(B) The contralateral side shows normal anatomy (arrow).
Fig. B31.4 (A) 3D TOF-MRA. Circle of Willis, coronal maximal intensity projection (MIP). Tailoring of the right C6-ICA with indication of vessel wall hematoma (arrows). Note the absence of right
A1-ACA (arrowhead). (B) MRI, T1-weighted fat-suppressed image,
axial plane. Increased signal intensity in projection of the C6-ICA
indicating vessel wall hematoma (arrowhead).
RL
Fig. B31.6 Schematic of the patient’s extra- and intracranial
brain-supplying arteries showing a hemodynamically irrelevant
stenosis in the right C6-ICA (circle).
442 Case 31 Dissection of the Right Internal Carotid Artery C6 Segment
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Follow-up Neuroradiologic Findings
(Day 120)
TOF-MRA revealed an almost normalized vessel
with only a mild tailoring of the distal C6-ICA. No
residual wall hematoma was seen on fat-suppressed
T1- weighted images (Fig. B31.7).
Clinical Course (2)
After 4 months, the patient remained with only residual
signs of reduced fi ne motor skills.
Final Diagnosis
Right-sided fragmented partial territorial MCA infarct
caused by artery-to-artery embolism in spontaneous intracranial but extradural C6-ICA dissecting stenosis with
almost complete restitution after 4 months (Fig. B31.7).
Aspirin medication was subsequently discontinued.
Discussion
Clinical Aspects
Here we describe a 46-year-old woman who sustained
small cortical infarcts within the territory of the right
MCA. A spontaneous C6-ICA dissection leading to
artery-to-artery embolic events was diagnosed.
Whenever brain ischemia is suspected, particularly
in young patients, cerebrovascular imaging should be
performed as soon as possible, preferentially using MR
diff usion-weighted images. Our patient had a fragment-
ed territorial MCA infarction which was missed by cranial CT. Territorial infarctions can be caused by distant
embolism and by in-situ thrombosis. The source of embolism may be the heart, the aortic arch, the extra- and
intracranial arteries, and leg veins in paradoxical events.
In elderly patients, almost all territorial brain infarcts are
of embolic etiology, mainly from the heart or from atherosclerotic vessel diseases. In young stroke patients, territorial infarction may also be of embolic origin but other
nonembolic causes like vasculitis, vasospasm, vasoconstriction, and nonatherosclerotic thrombosis have to be
considered.
Independent of etiology, brain-supplying vessels must
be meticulously examined as a potential cause of territorial infarction. If classic vascular risk factors are present
and the patient has suff ered, for instance, PCA stroke, the
two VA origins, the two V4-VA segments, the basilar artery
(BA), and the proximal ipsilateral PCA vessel segments are
the most likely potential sources of embolism. In patients
with typical vascular risk factors and MCA infarctions,
the ICA origin followed by the ICA siphon, terminal ICA,
M1-MCA, and proximal M2-MCA should be analyzed. In
patients without vascular risk factors and normal fi nd-
ings in the above-mentioned vessel segments, the petrosal C6-ICA should also be taken into consideration as it
is more often aff ected by atherosclerosis than previously
AB
Fig. B31.7 (A) 3D TOF-MRA. Circle of Willis, coronal MIP. Residual tailoring of the right C6-ICA after 4 months. The vessel wall
hematoma is completely resolved (arrows). (B) MRI, T1-weighted
fat-suppressed image, axial plane. Normalized vessel wall without
pathology in the C6-ICA segment (arrowhead).
assumed. In the INTRASTENT multicenter registry of 388
patients with intracranial stenoses, 13.9% of patients had
a lesion in the C6-ICA, which is only slightly lower than in
the carotid siphon (16.8%) and the MCA (18.6%) (Kurre et
al 2010). Therefore, all available ICA segments, including
C5-ICA and C6-ICA, have to be studied in patients with
ischemia of the anterior circulation, particularly if there
is no other detectable explanation.
Of note, we were able to detect the stenosis using
ultrasound but we could not explain its etiology. MRI
1 week after symptom onset confi rmed dissection of the
C6-ICA by revealing the wall hematoma (crescent sign) in
fat-suppressed T1-weighted images. If a typical wall hematoma is absent on MRI shortly after initial symptom
onset, e.g., on the fi rst two days, but dissection is suspect-
ed clinically, repeat MRI should be considered to better
delineate the wall hematoma. In our patient, the crescent
sign resolved and almost complete vessel restitution was
seen on a 4-month follow-up MRI. Vessel restitution is a
frequent fi nding and has been reported in ~70% within
the fi rst 3 months. Later regression is unusual but may
occur (Baracchini et al 2010, Nedeltchev et al 2009).
There are no evidence-based recommendations regarding medical therapy for the (1) acute phase, (2)
subacute phase, or (3) long-term secondary prevention
of dissection-induced stroke. According to the CADISS
trial, which enrolled 250 patients with extradural dissections, there was no statistically signifi cant diff erence
between oral anticoagulation and antiplatelet therapy in
terms of prevention of relapsing stroke or TIA (Markus et
al 2015). In our case, antiplatelet therapy was continued
after confi rming the diagnosis. Anticoagulation would
have exposed our patient to the risk of medicationinduced hematoma growth and secondary ICA occlusion.
Moreover, because MRA showed that the left A1-ACA
and left PCoA were absent, anticoagulation would have
substantially increased the risk of hemodynamic infarction. Secondary hematoma-induced vessel occlusion has
been described in patients receiving high-dose intravenous heparin (Dreier et al 2004). Though long-term
443Discussion
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
antiplatelet therapy was refused by our patient, it was
not medically indicated as he did not have any vascular
risk factors. For further reading on extracranial ICA dissection, see Case 11; for further reading on intracranial
dissection, see Case 21.
Angiologic and Anatomic Aspects
Dissections can be divided into traumatic and nontraumatic, aff ecting the ICA or VA in extracranial or intra-
cranial locations. The latter aspect is of importance for
treatment strategies, as anticoagulation is not recommended in intracranial dissections to avoid subarachnoid
hemorrhage (SAH). The risk of SAH, however, depends
on the vessel course in the subarachnoid space. Although
it is anatomically correct to assess this risk by diff eren-
tiating between an “extrasubarachnoid” and “intrasubarachnoid” location, it is more common to classify the
dissection location as extra- or intradural. The ICA penetrates the dura mater and arachnoid layer at the level of
the C2/C3-ICA near the origin of the ophthalmic artery. In
our case, the dissection site can be defi ned as intracranial
but extradural.
The C6 segment of the ICA (NB: radiologic nomenclature defi nes ICA segments according to the fl ow direc-
tion from its origin, i.e., the neurosonologic C6-ICA is the
r a d i o l o g i c C 2 - I C A ) c o r r e s p o n d s t o t h e p e t r o s a l p a r t o f t h e
ICA. It has a vertical section, extracranially accessible in
its most proximal part with the linear probe in submandibular position tilted cranially in a cross-sectional plane.
This vertical part is followed by a horizontal segment
which can be visualized using the transcranial phasearray probe analyzing the lower pontine insonation plane.
Provided that an appropriate ultrasound system is used,
identifi cation is particularly simple as no other relevant
arterial vessel is in the close vicinity of this straight vessel segment. Of note, TCD is not able to detect the C6-ICA
because of missing Doppler landmarks. For further reading on ultrasound anatomy of the C6-ICA, see Chapter 2,
“C6 Segment” of the internal carotid artery under “Special Arterial Anatomy and Ultrasound Anatomy.”
There are no published TCCS graduation criteria for
intracranial ICA stenosis. The Baumgartner criteria consider stenoses of the MCA, ACA, PCA, VA, and BA but
exclude the ICA, possibly because of the low number of
DSA-correlated ICA stenoses in the study or because of
the assumed tortuous vessel course. The latter might
be a problem for the segment of the ICA siphon; however, the terminal ICA and the C6-ICA have a straight
course which can be visualized in the coronal and axial
imaging planes. Angle-corrected fl ow velocity meas-
urements are also possible. In our case, stenosis was
confi rmed by MRA but also by comparing peak systolic
fl ow velocities of both sides which were obviously higher in the clinically symptomatic right C6-ICA (121 cm/s
v e r s u s 7 4 c m / s ) . T h e c u t - o ff velocity we use for identifi -
cation of a C6-ICA stenosis is a peak systolic velocity of
95 cm/s, derived from reported normal fl ow velocities
of 53 ± 14 cm/s (cut-off = mean + three standard devia-
tions) (Eggers et al 2009).
444
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
Case 32
Right Temporal Hemorrhage in Pial Arteriovenous Malformation
Clinical Presentation
A 32-year-old woman with no previous medical problems
presented with a generalized epileptic seizure and mild
headaches. She had no vascular risk factors except for
being a smoker. She did not take any regular medication
and did not have a known coagulopathy. On admission,
the neurologic examination revealed no focal neurologic
defi cits and no meningeal signs. Her blood pressure was
normal and drug screening was negative.
Initial Neuroradiologic Findings
Cranial CT on admission showed a right-sided temporal
intraparenchymal hemorrhage (IPH) (Fig. B32.1).
Suspected Diagnosis
Atypical right temporal IPH of unknown cause. A cerebral venous thrombosis (CVT), arteriovenous malformation (AVM), or dural arteriovenous fi stula (DAVF) was
considered.
Questions to Answer by Ultrasound
Techniques
velocity right 129/88 cm versus left 80/47 cm/s; PI right
0.40 versus left 0.58) (Fig. B32.2 and Fig. B32.3). The re-
maining intracranial arteries showed normal fl ow signals
with regular pulsatilities. Assessment of the intracranial
veins revealed normal fl ow signals and parameters in both
basal veins of Rosenthal (BVR), the great cerebral vein of
Galen (VG), the straight sinus (StS), and both transverse sinuses (TS) (not shown). In addition, a prominent arterial
and a venous fl ow signal were detected in the right corti-
cal/subcortical junction, insonated via the contralateral left
transtemporal bone (axial plane, insonation depth 98 mm:
arterial signal 149/103 cm/s, venous signal 96/70 cm/s).
Considering the location, the vessels were interpreted to
be a peripheral arterial feeder and venous recipient vessel
of an AVM (Fig. B32.4). Searching for more atypical vessels via the same insonation approach, another prominent
venous signal was detected at the subarachnoid/cortical
junction at a depth of 108 mm (fl ow velocity 38/27 cm/s)
(Fig. B32.5; see also Video
dus could be detected. Global cerebral circulation time was
not measured.
32.1). No circumscribed ni-
Conclusion
Suspected right-sided AVM in peripheral location with
the right MCA as main arterial feeder and drainage via
cortical veins.
• Were there signs of extracranial or intracranial feeding
arteries?
• Were there signs of extracranial or intracranial draining or collateral veins?
Initial Neurosonologic Findings
Extracranial Duplex Sonography
Duplex sonography revealed normal fi ndings in the ca-
rotid and vertebral arteries. In particular, both occipital
arteries (OccA) showed normal fl ow parameters. The in-
ternal jugular vein (IJV) and vertebral vein (VV) showed
normal fl ow signals on both sides.
Transcranial Duplex Sonography
Increased fl ow velocities with decreased pulsatility com-
pared with the contralateral side were observed in the
M1-segment of right middle cerebral artery (MCA) (fl ow
MRI, MR Angiography, and Dynamic
MR Angiography
MRI ruled out further bleedings. Time-of-fl ight MR angio-
graphy (TOF-MRA) showed prominent insular branches
of the right MCA and an enlarged cortical vein which
was also detectable upon review of the MRA raw data
(Fig. B32.6). MR venography was normal without signs of
CVT. Dynamic MRA fi nally proved the presence of a right
temporolateral AVM (Fig. B32.7).
Conventional Angiography
Digital subtraction angiography (DSA), performed to assess therapeutic options, confi rmed the fi ndings from
the dynamic MRA. In addition, a small feeder originating
from a right posterior cerebral artery (PCA) branch was
seen that had not been detected by the MRA (Fig. B32.8
and Fig. B32.9).
445Conventional Angiography
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
AB
Fig. B32.1 Cranial CT, axial plane (A) and coronal plane (B) revealing a circumscribed right temporal hematoma (arrows).
M1-MCA-L
M1-MCA-R
Fig. B32.2 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Mildly increased fl ow velocity and obvious decreased
PI in the right M1-MCA (fl ow velocity 129/88 cm/s, PI = 0.40).
M3-MCA-R
Fig. B32.3 TCCS ( tran stemp oral a ppro ach), right-sided insonation,
midbrain plane. Normal fl ow velocity and PI in the left M1-MCA at a
depth of 86 mm (fl ow velocity 80/47 cm/s, PI = 0.58).
Cortical vein R
Fig. B32.5 TCCS (transte mporal a ppro ach), left-sided insonation,
midbrain plane. Prominent venous vessel in the right temporal
c o r t i c a l r e g i o n a t a d e p t h o f 1 0 8 m m ( fl ow velocity 38/27 cm/s,
PI = 0.36). Arrows delineate the contralateral skull.
Fig. B32.4 TCCS (transte mporal approach), left-sided insonation,
midbrain plane. Raised flow velocity in an M3 branch of the right
MCA (flow velocity 149/103 cm/s, PI = 0.39) insonated together
with an assumed cortical vein with arterialized blood flow at a
depth of 98 mm (flow velocity 96/70 cm/s, PI = 0.33). Arrows
delineate the contralateral skull.
AB
Fig. B32.6 (A) 3D TOF-MRA, axial maximal intensity projection
(MIP). Prominent MCA insular branches and a vessel signal corresponding to a cortical vein (arrow). (B) Raw data MRA image revealing a prominent cortical MCA branch (arrowhead).
446 Case 32 Right Temporal Hemorrhage in Pial Arteriovenous Malformation
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
AB C
Fig. B32.7 Time-resolved dynamic MRA, coronal MIP: Ultra-early
arterial phase (A), early arterial phase (B), venous phase (C). In A
and B the AVM nidus is visualized in both early arterial phases (red
circle). Also note an early parietal vein (arrow) and a frontal vein
(arrowhead).
Fig. B32.9 DSA, left vertebral artery (VA) injection, posteroanterior view, arterial phase. Small feeder originating from a temporal
branch of the PCA (arrowhead) fi lling the pial AVM (red circle).
(Courtesy of Prof. Fiehler, Neuroradiological Department, University Hospital Eppendorf, Hamburg, Germany.)
Fig. B32.8 DSA, right internal carotid artery (ICA) injection, posteroanterior view, early arterial phase. Note the pial AVM (red circle) and the prominent parietal (large arrowhead) and frontal vein
(small arrowhead). (Courtesy of Prof. Fiehler, Neuroradiological
Department, University Hospital Eppendorf, Hamburg, Germany.)
AB
Fig. B32.10 3D TOF-MRA, axial MIP. (A) Findings before surgery
with prominent AVM-related vessels. (B) Follow-up image after
surgical AVM resection with normalized fl ow signals (red circle).
(Courtesy of Prof. Fiehler, Neuroradiological Department, University Hospital Eppendorf, Hamburg, Germany.)
Clinical Course
Because of the peripheral location, surgery was considered to be the best treatment option. AVM extirpation
was subsequently performed without complication. The
postsurgical MRA was unremarkable (Fig. B32.10). Antiepileptic treatment was recommended for 6 months.
Ultrasound follow-up was not performed.
Final Diagnosis
Symptomatic left temporolateral IPH caused by a
right-sided pial AVM, mainly fed by the MCA. Successful
surgical resection.
Discussion
Clinical Aspects
Here we report on a 31-year-old woman with an intraparenchymal hemorrhage (IPH). She had no known vascular
risk factors. She denied drug abuse, which was confi rmed
by a negative toxicological screening test. Drug-related
IPH also seemed unlikely because of the location of the
bleeding site, which, as in chronic hypertensive patients,
would be expected to be subcortical (Sloan 2009).
IPH accounts for ~10% of all strokes and results from
a wide spectrum of disorders (Qureshi et al 2009, Rønning et al 2008). The most common cause is arterial
447Discussion
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
All rights reserved. Usage subject to terms and conditions of license.
h y p e r t e n s i o n , c o m m o n l y a ff ecting middle-aged patients
with often long-standing arterial hypertension. The bleeding is then typically located in the basal ganglia, thalamus,
internal capsule, deep periventricular white matter, pons,
or subcortical cerebellum. The main cause is a small vessel
alteration, due to hypertension, and rupture.
Our patient had a peripherally located IPH, which may be
referred to as a lobar hematoma. Lobar hematoma is a common fi nding in cerebral amyloid angiopathy (CAA) which
usually aff ects elderly patients >70 years (Charidimou et
al 2012). Considering demographic data and the improved
hypertension control in the population, amyloid-related
bleeding is becoming a more important consideration in
developed countries. However, our patient was too young
for this condition. Less common causes of nontraumatic hematomas in a mostly lobar location are infections, tumors,
acquired or congenital coagulopathies, and arteriovenous
malformations. The most frequently observed acquired
coagulopathies result from the therapeutic use of aspirin
and anticoagulants. If used, they may additionally add to
the risk of bleeding caused, for instance, by hypertension
or CAA. Other acquired coagulopathies that may cause
IPH include bleeding dyscrasias secondary to neoplasms
(e.g., leukemia), idiopathic thrombocytopenic purpura, and
thrombocytopenia induced by alcohol or liver and kidney
disease. None of the above conditions were present in our
case. For completeness, other rare conditions and congenital causes like hemophilia A and B must be mentioned
(Donahue et al 1986, Kase et al 1990, Lee and Kim 1998).
Herpes simplex encephalitis (HSE) may be a more relevant
diff erential diagnosis, as a hemorrhagic transformation may
resemble bleeding. Its typical location, however, is the temporomesial area and insula, neither of which was aff ected in
our case. Furthermore other supportive signs of HSE, such
as headache, meningeal signs, and fever were also missing
(Rodríguez-Sainz et al 2013).
A hemorrhage located in the temporal lobe may also
be caused by CVT if the drainage of the transverse sinus
and of the vein of Labbé is blocked. Our patient had suffered from mild headaches but sinus or isolated venous
thrombosis was not assumed by ultrasound and was excluded by MR venography (for further discussion on CVT,
see Case 29).
Finally, a vascular malformation was identifi ed as the
cause of the patient’s lobar hemorrhage. In the course
of the diagnostic process, ultrasound was indicative of
an arteriovenous shunt because of the detectable corresponding typical arterial and venous fl ow signals. MRA
and DSA then confi rmed this fi nding by demonstrating a
pial AVM with a small nidus fed by the MCA and partially
by the ipsilateral PCA (for further reading on DAVF, see
Case 34; for further reading on AVM, see Case 4 and Case
40). Surgical resection was performed because of the
symptomatic bleeding and the subsequently increased
risk of a second event as well as a presumably low risk of
surgery with the superfi cial angioma location (Spetzler–
Martin grade only 1 point).
Angiologic and Anatomic Aspects
Ultrasound is an excellent noninvasive method for
detection of AVMs, especially in cases with high-fl ow
shunts. It is important to include not only traditional
parameters like arterial fl ow velocity and pulsatility
but also venous fl ow signals. When in doubt, shunt
assessment by means of cerebral circulation time may
be of help. In our case, extracranial arterial and venous
fi ndings were completely normal, excluding a high
shunt volume but not the presence of a shunt itself. Intracranial examination revealed an increased fl ow ve-
locity in the right MCA with low pulsatility, indicating
hyperperfusion and therefore suggesting an AVM feeding function. The more distal the insonated segment,
i.e., the closer to the AVM nidus, the lower the pulsatility as it is directly dependent on the cerebrovascular resistance. Flow velocity in the feeding arteries may vary
and is often most prominently increased in a proximal
location. However, high velocities may also be detected
near the nidus.
In our case, the M3-MCA feeder revealed not only
a lower pulsatility but also higher velocities than the
M1-MCA main stem itself. In the draining vessels, a
reversed pattern can be observed. The general rule
applies here—namely, the closer to the nidus a feeder
is, the lower the pulsatility and vice versa; the farther
away, the higher the observed velocity and pulsatility.
Directly at the nidus, arterial and venous vessel signals are almost identical and a clear diff erentiation
between them may not be possible. In suspected AVM,
the assumed feeder should be followed to the most
distal accessible location. In our case, we analyzed the
cortical vessels near the skull by insonation from the
contralateral side. This approach is also recommended
for the examination of the transverse sinus (see also
Chapter 2, “Confl uence of Sinuses [CoS], Transverse Si-
nus [TS], and Superior Sagittal Sinus [SSS]” under “Special Venous Anatomy and Ultrasound Anatomy”) as well
as for B-mode insonation of subdural and intraparenchymal hemorrhages (see also Chapter 5, “Intracranial
Hemorrhage” under “Intracranial Stroke-related B-mode
Pathology”).
The small feeder originating from the right PCA,
probably representing the anterior temporal or occipitotemporal artery, was not identifi ed by transcranial
color-coded duplex sonography (TCCS). The PCA main
stem in our patient revealed comparable fl ow veloci-
ties and pulsatilities on both sides and no special analysis of the PCA branches was performed. However, if
examined, typical feeder fl ow characteristics with low
pulsatility and increased fl ow velocities compared with
the contralateral side would have been expected, compatible with a low fl ow contribution by the PCA. For
further reading on ultrasound fi ndings in angiomas,
see Case 4 and Case 40; for ultrasound fi ndings in dural
fi stula, see Case 34.
448
Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers
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Case 33
Subarachnoid Hemorrhage after Rupture of Left Supraophthalmic
Internal Carotid Artery Aneurysm
Clinical Presentation
A 42-year-old woman was admitted to the emergency department. The patient’s family reported that she had suffered a sudden onset of very severe headache and nausea.
The ambulance was called immediately. The emergency
physician diagnosed drowsiness, confusion, and meningism.
Shortly after hospital admission her vigilance progressively
declined further, requiring intubation and mechanical ventilation (Glasgow Coma Scale 8). Seventeen years previously
the patient had suff ered from a mild subarachnoid hemor-
rhage (SAH) caused by a left-sided intradural internal carotid artery (ICA) aneurysm located at the junction of the
posterior communicating artery (PCoA). Aneurysm clipping
was done without complication at that time. No follow-up
examinations were performed. The family history and medical history were otherwise unremarkable.
Initial Neuroradiologic Findings
Noncontrast cranial CT showed a diff use bleeding in the
subarachnoid space of >1 mm thickness without intraventricular or intracerebral clots (Fisher grade 3). The
CT also revealed signs of increased intracranial pressure
(ICP) (Fig. B33.1A). CT angiography (CTA) demonstrated a
fusiform supraophthalmic left ICA aneurysm as the most
probable source of bleeding (Fig. B33.1B).
Conventional Angiography
Digital subtraction angiography (DSA) confi rmed the left
ICA aneurysm (diameter 11 × 9.6 × 7.2 mm) at the junction of the PCoA with an irregular confi guration as the
source of the SAH (Fig. B33.2).
lowing day without complications. Afterwards the patient
was transferred to the neurosurgical intensive care unit
(ICU). A second CT on the same day showed no detectable
changes (not shown).
Questions to Answer by Ultrasound
Techniques
• Was there evidence of cerebral vasospasm (VS) of the
basal cerebral arteries in the course of disease?
• Were there signs of cerebral hyperperfusion in the course
of disease, or a mixture of hyperperfusion and VS?
• In case of VS, is there any dynamic change over time?
Initial Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
No macroangiopathic changes. Normal angle-corrected
s y s t o l i c fl ow velocities were detected in the left ICA
(53 cm/s). The right ICA was not measurable due to a central
venous catheter in the internal jugular vein (Fig. B33.3).
Transcranial Duplex Sonography
All transcranial measurements, initially and during the
follow-up examinations, were performed without angle
correction. Normal fl ow velocities in the lower range were
seen in the middle cerebral artery (MCA), anterior cerebral
artery (ACA), and posterior cerebral artery (PCA) in their
fi rst and second segments as well as in the intracranial ICA.
Normal fl ow velocities were also seen in both basal veins
of Rosenthal (BVRs). On the left side the MCA/ICA ratio—
using the M1 part of the MCA, the extracranial part of the
ICA, and systolic fl ow velocities—was 1.3 and the MCA/BVR
ratio was 5 (Figs. B33.4–B33.9).
Diagnosis
Severe SAH grade IV according to the Hunt & Hess grading
system (Hunt and Hess 1968) and grade III according to Fisher et al (1980) after rupture of a left-sided supraophthalmic
ICA aneurysm treated surgically by clipping 17 years before.
Conclusion
Normal extracranial and intracranial fl ow parameters
without evidence of cerebral hyperperfusion or VS.
Neurosonologic Findings (Day 3 to Day 5)
Extracranial Duplex Sonography
Clinical Course (1)
An external ventricular drainage was implanted immediately after the CT scan for continuous monitoring and
management of ICP. Coil occlusion was performed the fol-
Daily measurements showed normal fl ow velocities
throughout the observational period. The highest systolic
fl ow velocity seen in the left ICA was 82 cm/s on day 5
(not shown).
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