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209Discussion
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.
generation and therefore carries the risk of incomplete
thrombus visualization. Thus, source data review is mandatory when assessing MRA. This likewise applies to CTA,
in which MIP is also used for data postprocessing. However, here source data evaluation is already established as
all high-resolution cross-sectional images are analyzed
regularly. Currently, dynamic information concerning
potential thrombus movement is not provided. However,
the 360° circumference of the thrombus can be depicted,
and allows identifi cation, for example, of apical thrombus
segments without vessel wall adhesion, likely to be of
fl oating character. CTA may also have problems in distinguishing FFT from ulcerated plaques, both characterized
by fi lling defects (Jaberi et al 2014).
Our case underlines that knowledge of the vascular
status, for example, derived from a neurosonologic investigation, is of particular interest as it may allow selection
of patients for intravenous thrombolysis or other therapeutic strategies on the basis of the underlying vascular
pathology (Gerriets et al 2000).
210
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 3
Left Common Carotid Artery Occlusion
Clinical Presentation
A 64-year-old man was admitted with a transient
right-sided facial paresis that had lasted a few minutes. At the same time he experienced some slurring
of his speech as well as diffi culty fi nding appropriate
words. The symptoms started while he was standing
in his kitchen, preparing breakfast. Six years earlier, he
had had an ischemic brain infarction with right-sided
hemiparesis. An artery-to-artery embolism was suspected due to symptomatic internal carotid artery
(ICA) stenosis, and a carotid endarterectomy (CEA) was
performed. At this time, long-term secondary stroke
prevention was started with daily aspirin. Follow-up
several weeks after the surgery revealed complete
occlusion of the common carotid artery (CCA) and ICA
on the operated side. The patient had no history of vascular risk factors, particularly no arterial hypertension,
and he was not taking any other medication.
Initial Neuroradiologic Findings
Cerebral MRI showed old ischemic brain lesions in the left
middle cerebral artery (MCA) and anterior cerebral artery
(ACA) territories. In addition, multiple small focal lesions
were found in the right hemisphere. However, there were
no signs of acute cerebral ischemia in the diff usion-weight-
ed MR images. The cervical contrast-enhanced magnetic
resonance angiogram (MRA) showed no contrast in the left
CCA, ICA, and external carotid artery (ECA). Regular signal
intensities were present within the right carotid arteries
and the vertebral arteries (VAs) (Fig. B3.1 and Fig. B3.2).
Suspected Diagnosis
Left hemispheric transient ischemic attack (TIA) of
hemodynamic origin.
Initial Neurosonologic Findings
Extracranial Duplex Sonography
B-mode sonography revealed distinct atherosclerotic vascular changes, particularly in the right carotid bifurcation. The right CCA revealed a mildly increased velocity of
128/33 cm/s. Doppler spectrum analysis showed no signal
in the left CCA, ICA, and ECA. The lumen of the left CCA was
small and completely fi lled with moderate hyperechoic
material, consistent with an old occlusion. Assessment of
the VAs was normal (Fig. B3.3, Fig. B3.4, Fig. B3.5).
Transcranial Duplex Sonography
A poststenotic fl ow pattern was seen in the left M1
segment of the MCA with an oscillation eff ect following
digital tapping of the contralateral ICA at the submandibular level. No fl ow signal was seen in the intracranial
segment of the left distal ICA. The left A1 segment of the
anterior cerebral artery (ACA) fl ow direction was retro-
grade due to cross-fl ow from the contralateral ICA. In the
ACoA (depth 72 mm) an increased fl ow velocity and tur-
bulence was detected, indicative of a functional stenosis.
Flow in the right A1-ACA segment was slightly increased
(fl ow velocity 135/65 cm/s) but not turbulent. Compar-
ing both P1- and P2-PCA segments, a mild increased fl ow
velocity was seen on the left side. The left ophthalmic artery (OA) could not be detected transorbitally (Figs. B3.6–
B3.12; see also Videos
Conclusion
• Extracranial occlusion of the left common, internal,
and external carotid arteries.
• Intracranial collateral blood fl ow into the left MCA
and ACA territory via ACoA and via leptomeningeal
collaterals of the PCA.
B3.1 and B3.2).
Questions to Answer by Ultrasound
Techniques
• Was there evidence of occlusion or near occlusion of
the left CCA or ICA?
• If so, was there evidence of collateral blood fl ow via
the anterior communicating artery (ACoA) and posterior communicating artery (PCoA) or leptomeningeal
vessels via the posterior cerebral artery (PCA)?
Fig. B3.13 and Fig. B3.14 show schematics of the ex-
tra- and intracranial brain-supplying arteries of a healthy
subject and of the patient, respectively.
Clinical Course
The acute clinical symptoms in our patient suggested a TIA
in the left cerebral hemisphere. Neurosonologic fi ndings
211Discussion
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.
Fig. B3.1 MR FLAIR image, axial plane. Old MCA infarction in the
left central region (arrow).
CCA-R
Fig. B3.3 Extracranial duplex, longitudinal plane. Mild increase of
fl ow velocity in the right CCA (fl ow velocity 128/33 cm/s) which can
be interpreted as sign of collateral fl ow.
confi rmed the already known left CCA and ICA occlusion
which excluded an embolic event and argued in favor of a
hemodynamic event. The 24-hour blood pressure recordings did not demonstrate hypotensive episodes. To assess
the risk for further hemodynamically induced ischemic episodes, an acetazolamide test (see also Chapter 3,
“Acetazolamide Infusion Test” under “Metabolic Coupling”)
was performed. Intravenous administration of 1 g acetazolamide led to a 23.4% increase of right MCA fl ow velocity
and a less prominent fl ow velocity increase in the left MCA
of 10.2%, but this was still within the normal range. As a result of these fi ndings and in the absence of recent cerebral
ischemia on MRI, it was decided to keep the patient under
regular follow-up and no medication changes were made.
He remained stable with no further ischemic attacks over
a follow-up period of 4 years.
Fig. B3.2 Contrast-enhanced 3D MRA, coronal MIP. No signals in
the left common, internal, and external carotid arteries.
CCA-L
Fig. B3.4 Extracranial duplex, longitudinal plane (B-mode image): The
narrowed lumen of the left CCA is completely fi lled with moderate
echogenic material indicating a nonacute occlusion (arrows).
Final Diagnosis
Hemodynamic TIA in the left hemisphere caused by
persisting CCA and ICA occlusion.
Discussion
Clinical Aspects
The subject is a 64-year-old male patient with radiologic fi ndings of a left CCA occlusion. Six years prior
to this episode he underwent CEA because of a symptomatic left ICA stenosis. Some weeks after the CEA a
complete left CCA and ICA occlusion was noted which
remained asymptomatic until now, when he presented
with a left hemispheric TIA.
212 Case 3 Left Common Carotid Artery Occlusion
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.
CCA-L
Fig. B3.5 Extracranial duplex, longitudinal plane. Doppler spectrum analysis shows no fl ow in the left CCA consistent with an oc-
clusion. Note the preserved fl ow signal of the internal jugular vein
above the CCA.
M1-MCA-R
M1-MCA-L
Fig. B3.6 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
midbrain plane: Mild poststenotic fl ow pattern in the left M1-MCA
mainly indicated by a relative increase of the diastolic blood fl ow
(fl ow velocity 70/34 cm/s).
A1-ACA-L
Fig. B3.7 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
midbrain plane. Normal fl ow signal in the right M1-MCA at a depth
of 103 mm (fl ow velocity 92/37 cm/s). Note: the insonation was
performed from the contralateral side.
CCA occlusions are fairly rare. In a stroke population
they present with an incidence of ~2% (Hass et al 1968,
Riles et al 1984). In comparison with ICA occlusion,
symptoms, etiology, and pathogenesis of CCA occlusion
are rarely discussed. Clinically, CCA occlusions can occur
without symptoms but may also lead to ischemic stroke
with severe neurologic defi cits (Podore et al 1981). A
small case series reported orthostatic-related clinical
symptoms in two-thirds of 17 patients. TIAs were reported in 82% of cases. Completed stroke occurred in 59% of
patients (Levine and Welch 1989). Most of the strokes in
CCA occlusion were major (Chang et al 1995). Another
series, including 20 patients, showed symptomatic occlusion in 80%. Here in 65% of cases the right CCA was
aff ected, only one patient revealed a bilateral occlusion
(Bajko et al 2013).
The etiology of CCA occlusions is mostly atherosclerotic in white patients, but other causes have to be considered. In a series of 44 Asian patients, Takayasu’s arteritis
was found in 25% of cases, postradiation angiopathy in
Fig. B3.8 TCCS (transt empo ral approac h), left -sided inso nation, midbrain plane. Reversed fl ow direction in the left A1-ACA
with mild turbulence caused by the cross-fl ow via the ACoA (fl ow
velocity 85/30 cm/s).
16%, and cardioembolic events in 14% (C.F. Tsai et al 2005).
The prevalence of Takayasu’s arteritis is particularly high
in the Asian population. Furthermore, the occurrence of
nasopharyngeal carcinomas and their subsequent treatment with radiation therapy of the neck are associated
with a higher incidence of CCA occlusion in the Chinese
and Taiwanese populations.
In our reported case, the occlusion occurred within
several weeks after an accomplished CEA. Early restenosis as a complication of the above procedure does occur,
as has been studied in the ACAS trial on 645 patients
with completed ultrasound data. Depending on the surgical technique used an early restenosis (<18 months) occurred in 7.6–11.4%, and a late restenosis (18–60 months)
was observed in only 1.9–4.9% of cases. Notably, in this
study no specifi c risk factor, especially continued tobacco
use or hyperlipidemia, was associated with a higher incidence of recurrent carotid stenosis (Moore et al 1998). A
postinterventional vessel occlusion was not reported in
this trial, but has been observed in older studies at least
213Discussion
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.
A1-ACA-R
Fig. B3.9 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Increased but nonturbulent fl ow in the right
A 1 - A C A ( fl ow velocity 135/65 cm/s).
P1-PCA-L
ACoA
Fig. B3.10 TCCS (tran stemporal appro ach) , left -sid ed ins onati on,
midbrain plane. Increased fl ow velocity with turbulence, indicating
a functional stenosis of the ACoA (fl ow velocity 150/80 cm/s).
P1-PCA-R
Fig. B3.11 TCCS (tran stemporal appro ach) , left -sid ed ins onati on,
midbrain plane. Increased fl ow velocity in the left P1-PCA (fl ow
velocity 97/40 cm/s).
Fig. B3.12 TCCS (tran stemporal appro ach) , left -sid ed ins onati on,
midbrain plane. Normal fl ow velocity in the right P1-PCA (fl ow
v e l o c i t y 7 3 / 3 5 c m / s ) . N o t e : t h e i n s o n a t i o n w a s p e r f o r m e d f r o m t h e
contralateral side.
214 Case 3 Left Common Carotid Artery Occlusion
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.
1
2
3
12
13
4
5
6
7
8
9
10
11
RL
Fig. B3.13 Schematic of the extra- and intracranial brain-supplying
arteries. Red: Right-sided anterior circulation. Blue: Left-sided anterior circulation. Green: Posterior circulation. Pink: ACoA and PCoA.
1 = A CoA; 2 = A 2-A CA; 3 = A 1-A CA; 4 = early temporal M1-MCA
branch; 5 = M1-MCA; 6 = PCoA; 7 = P1-PCA; 8 = P2-PCA; 9 = ICA;
10 = ECA; 11 = CCA; 12 = lenticulostriate arteries; 13 = M2-MCA;
14 = OA; 15 = SCA; 16 = A ICA; 17 = BA; 18 = PICA; 19 = V4-VA;
20 = V3-VA; 21 = V2-VA; 22 = SA.
14
15
16
17
18
19
20
21
22
In contrast, one-half of the patients with occluded distal
vessels presented with a major stroke in a series of 21 patients (Zbornikova and Lassvik 1991).
Data regarding treatment strategies is scarce and heterogeneous. Surgical reopening is not attempted. Instead,
in cases of severely impaired cerebrovascular reactivity
due to insuffi cient collaterals and reoccurring hemo-
dynamic ischemic events, an extracranial–intracranial
(EC – IC) bypass operation can be considered (Belkin et al
1993) (for further discussion on EC–IC bypass, see Case
25). Another surgical treatment option has been reported
in a recently published review. Here 94% of 146 patients
suff ered from symptomatic CCA occlusion. More than 70%
had an open ICA, and 80% of them were treated surgically
with a subclavian artery–ICA bypass. The rate of postoperative ipsilateral stroke in the fi rst 30 days was 1.5% and
nine patients (6.6%) had cerebral ischemia within a mean
follow-up of 25.6 months. This surgical option reveals a
low perioperative cerebrovascular morbidity and may be
of interest in a symptomatic patient with severely compromised collateral circulation (Klonaris et al 2013).
Angiologic and Anatomic Aspects
Diagnosis and classifi cation of a CCA occlusion with
extracranial duplex ultrasound is simple and reliable.
Furthermore, ultrasound echogenicity analysis of the
intraluminal thrombotic material allows one to draw
conclusions about the etiology of the occlusion. If
atherosclerotic vessel wall changes are present in the
extracranial arteries, and the thrombus itself is hyperechoic or of heterogeneous echogenicity, an atherosclerotic cause is very likely. In cases of cardioembolic
occlusions or in-situ thrombosis, the thrombotic material appears hypoechoic and may even show fl oating
RL
Fig. B3.14 Schematic of the patient’s extra- and intracranial
brain-supplying arteries. Note the occlusion of the left CCA, ICA,
and ECA (circle). Blood supply of the left MCA and ACA territory is
via the ACoA. Additional leptomeningeal collateralization of the left
MCA territory comes from the left PCA (green arrow).
parts (C.F. Tsai et al 2005). A complete resolution within at least several weeks and usually more rapidly has
then to be expected in embolic cases.
Intracranial compensation of a CCA occlusion (i.e., for
the ipsilateral ACA and MCA territory) requires competent and eff ective collateral pathways, similar to the ICA
occlusion. The quality of the collateral pathways fi nally
determines the extent and severity of the brain damage.
This is especially true if an acute occlusion occurs.
Tra nsc rania l ult ras oun d perm its excell ent o ppo rtun ities to evaluate all potential collateral pathways. In the
presented case with a type II occlusion of the CCA including the ipsilateral ICA, a typical collateral pattern is
seen. The main collateral blood supply of the left cerebral
hemisphere occurs from the right ICA via the A1-ACA, anterior communicating artery (ACoA), and retrograde left
A1-ACA into the left MCA territory. In our patient, a crossfl ow was easily depicted because of the excellent acoustic
temporal bone window. A cross-fl ow was also assured by
the applied submandibular tapping of the contralateral
ICA, which leads to typical fl ow transients on the MCA
of the occluded side. This tap test may be of help in patients with limited insonation quality to assess the collateralization pattern. The slightly increased fl ow within
the right CCA (contralateral to the side of the occlusion)
indicates the intracranial cross-fl ow during extracranial
ultrasound examination. Intracranially, bilateral comparison of the P1- and P2-PCA segments demonstrates
a slight left-sided fl ow increase, indicating additional
leptomeningeal collateralization via the PCA territory. In
type I CCA occlusion in most cases both the ECA and ICA
remain open. Here duplex ultrasound allows confi dently
the analysis of the extracranial fl ow pathways and fl ow
quantity (see also Chapter 5, “CCA Stenosis and Occlusion” under “Extracranial Pathology”).
Case 4
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.
Left Temporal Arteriovenous Malformation
215
Clinical Presentation
A 45-year-old man presented with recurrent episodes of
impaired consciousness followed by a confusional state
lasting for several minutes. On hospital admission his
neurologic examination was normal.
Initial Neuroradiologic Findings
Cerebral MRI showed a lesion (30 × 25 mm) with
numerous fl ow voids in the left temporal region extending
temporomesially and showing intense enhancement on
postgadolinium MRI. There were no signs of recurrent
bleeding. An enlarged draining vein running along the
left midbrain was interpreted as a dilated basal vein of
Rosenthal (Fig. B4.1). MR angiography (MRA) was not
performed.
Suspected Diagnosis
Repeated complex partial seizures caused by an arteriovenous malformation (AVM) in the left temporal lobe.
Questions to Answer by Ultrasound
Techniques
of the left middle cerebral artery (MCA) and posterior
cerebral artery (PCA) considered to be the nidus of the
AVM . Cle ar ide ntifi cation of the terminal ICA and the
proximal MCA was not possible. An arterial vessel signal away from the probe with turbulent fl ow, increased
fl ow velocity, and reduced PI related to the vessel conglomerate was thought to represent a major feeder originating from the distal ICA (fl ow velocity 155/84 cm/s).
More posteriorly, a similar feeder signal with a marked
turbulent fl ow and musical murmurs toward the probe
and a reduced PI was found in the projection of the left
proximal P2-PCA segment (fl ow velocity 150/78 cm/s).
The distal left M1-MCA as well as the distal left P2- and
P3-PCA segments revealed normal fl ow velocities and
PI. Raised fl ow velocities with an increased PI were
observed in the enlarged left basal vein of Rosenthal
(fl ow velocity 52/30 cm/s) but not in the contralat-
eral corresponding vein (fl ow velocity 13/10 cm/s;
Figs. B4.4–B4.11; Videos
graphic measurement of the global cerebral circulation
time between the left ICA and the left internal jugular
vein (IJV) after intravenous administration of an echo
contrast agent (Levovist) was signifi cantly shortened
(3.4 seconds compared with the normal published value of 7 ± 1.3 seconds; see Video
discussion, see Chapter 3, “Cerebral Circulation Time”
under “Parameter s of Cerebral Hemodynamics.”
B4.1–B4.3). Duplex sono-
B4.4). For further
• Detection of the nidus.
• Detection of the feeding arteries.
• Detection and identifi cation of the draining veins.
Initial Neurosonologic Findings
Conclusion
Large left temporal AVM. Blood supply via feeding arteries from the left distal ICA or proximal M1-MCA and left
proximal P2-PCA segments. Main drainage via the left basal vein of Rosenthal. Signifi cant shortening of the global
cerebral circulation time.
Extracranial Duplex Sonography
Comparison of the right and left sides revealed increased
fl ow velocity in the left internal carotid artery (ICA) and
reduced pulsatility (fl ow velocity / pulsatility index (PI):
left ICA 81/48 cm/s / 0.6; right ICA 59/24 cm/s / 0.95).
Assessment of both vertebral arteries (VAs) was normal
(Fig. B4.2
and Fig. B4.3).
Transcranial Duplex Sonography
Color-mode imaging revealed atypical fl ow signals of
multiple vessels (25 × 25 mm) between the main stem
Conventional Angiography
Digital subtraction angiography (DSA) was performed
which confi rmed an AVM with a nidus of 30 × 25 × 15 mm
visible on selective left ICA injection. The main feeder
was the anterior choroidal artery. AVM supply during
vertebral contrast injection was seen via the posterior
choroidal artery from the proximal PCA. Extensive fi ll-
ing of the dilated left basal vein of Rosenthal, followed
by the straight sinus, was seen even in the early arterial
phase of the carotid and vertebral angiograms (Fig. B4.12,
Fig. B4.13, Fig. B4.14).
216 Case 4 Left Temporal 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.
Fig. B4.1 MR T2-weighted image, axial plane. Multiple fl ow voids
in the left temporal lobe corresponding to the nidus of the AVM.
Note the enlarged basal vein of Rosenthal as a major AVM draining
vein (arrowhead).
ICA-L
Fig. B4.2 Extracranial duplex, longitudinal plane. Left ICA with
slight increase of blood volume fl ow (330 mL/min) and fl ow
velocity (81/48 cm/s) and reduced pulsatility in comparison to the
contralateral side (PI = 0.6).
AVM
ICA-R
Fig. B4.3 Extracranial duplex, longitudinal plane. Right ICA with
lower blood volume fl ow (220 mL/min). Normal fl ow velocity
(59/24 cm/s) and pulsatility (PI = 0.95).
Clinical Course
Because of the reported recurrent complex partial seizures, anticonvulsive therapy was started. Opinions
were obtained from our neurosurgeons, interventional
neuroradiologists, and radiotherapists. Microsurgical
resection was considered to be of high risk because of
the eloquent localization of the malformation. Radiosurgery was not indicated because of the large size of the
AVM . Parti al emb oli zat ion wa s con sid ered to be poss ibl e
Fig. B4.4 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
midbrain plane. AVM nidus in the left temporal lobe refl ected
by the multicolored signals indicating diff erent fl ow directions
(arrowhead). Note the course of the M1-MCA (arrows) as well as
the A1-ACA (arrow).
via the endovascular approach; however, the patient
decided against any intervention. Repeated clinical and
ultrasound follow-up over an observational period of
12 years showed no further changes. No further seizures
have occurred to date.
Final Diagnosis
Symptomatic epilepsy with co mplex partial seizures
caused by a left temporal AVM.
217Final Diagnosis
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.
AVM
Fig. B4.5 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
thalamic plane. The AVM nidus (arrowhead) appears larger in the
thalamic plane and the draining basal vein of Rosenthal becomes
visible (arrow).
M1-MCA-L
Feeder from distal ICA-L
Fig. B4.6 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
midbrain plane. Increased velocity and turbulent fl ow away from
the probe in projection of the terminal ICA corresponding to an
AVM feeder (fl ow velocity 155/84 cm/s, reduced PI = 0.66).
Feeder from P2-PCA-L
Fig. B4.7 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
midbrain plane. Normal fl ow signal in the distal left M1-MCA (fl ow
velocity 109/40 cm/s, normal PI =1.1).
P2-PCA-L
Fig. B4.9 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
thalamic plane. Normal fl ow velocity in the distal left P2-PCA (fl ow
velocity 66/29 cm/s, normal PI = 0.9). Note the hidden fl ow signal
of the basal vein of Rosenthal within the spectrum of the PCA.
Fig. B4.8 TCCS ( tran stemp oral appro ach) , le ft-s ided inson atio n,
midbrain plane. Increased fl ow velocity in the proximal left P2-PCA
toward the probe corresponding to an AVM feeder (fl ow velocity
150/78 cm/s, reduced PI = 0.71).
BVR-L
Fig. B4.10 TCCS (tran stemporal appro ach) , left -sid ed ins onati on,
thalamic plane. Left basal vein of Rosenthal with increased fl ow
velocity and “arterialized” fl ow signal (fl ow velocity 52/33 cm/s,
increased PI = 0.48).
218 Case 4 Left Temporal 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.
BVR-R
Fig. B4.11 TCCS (t rans tempora l ap proach) , right-s ided inso nati on,
thalamic plane. Normal fl ow signal in the right basal vein of Rosen-
thal (fl ow velocity 13/10 cm/s, normal PI = 0.27). Note the fl ow sig-
nal of the normal right P2-PCA in the background.
Fig. B4.12 DSA, left ICA injection, posteroanterior view. Contrast
fi lling of a convoluted vessel mainly via the anterior choroidal artery
(selective angiogram, not shown). Note the prominent basal vein
of Rosenthal already seen in the arterial phase surrounding the
midbrain (arrows).
Fig. B4.13 DSA, left ICA injection, lateral view. A similar picture is
seen in the lateral view. Note again the early visualization of the
prominent basal vein of Rosenthal (arrows).
Discussion
Clinical Aspects
We have described a patient with symptomatic epilepsy
suff ering from complex partial seizures due to a left tem-
poral AVM in the hippocampal area. Seizures unrelated to
hemorrhage are the second most common symptom at
Fig. B4.14 DSA, left VA injection, posteroanterior view: Filling of the
AVM via th e prox imal P CA an d its bran ches . No rel evan t opac ifi ca-
tion of the distal PCA because of suction of the main contrast agent
into the AVM. Note the prominent basal vein of Rosenthal (arrows).
initial presentation in patients with AVM. An analysis of
1,289 patients with AVM from three centers found focal
seizures in 8–12% and generalized seizures in 27–35% of
cases (Hofmeister et al 2000). Predisposing factors include
male sex, AVM size, frontal lobe and arterial border zone
location (Stapf et al 2000). Furthermore, in a prospective
study all patients with seizures at initial presentation
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