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Case 2 Free-floating Thrombus of the Extracranial Internal Carotid Artery
136
Degree of Neurosonologic Difficulty: Low
Fig. B2.9 Intraoperative view. Thrombus in the left proximal ICA. Fig. B2.10 Extracranial duplex, longitudinal plane. Left carotid bi-
Aside from the underlying hematologic disease, Sjögren
syndrome was present in our patient and was being managed with steroids. Up to one-third of patients with
Sjögren syndrome are known to have antiphospholipid
antibodies (Fauchais et al. 2004), which are a known cause
of acquired hypercoagulability. In fact, the antiphospholipid antibody syndrome is more common than any inherited coagulopathy. In this condition venous and arterial
thrombi are equally common (Thomas 2001). In our patient, the anticardiolipin antibodies were negative. However, the steroid treatment could still have promoted a
prothrombotic constellation.
Finally, our patient presented with anemia and thrombocytosis, which can both be associated with thrombus
formation in the carotid arteries in patients without identifiable macrovascular disease (Akins 1996). Generally,
thrombus formation requires platelet activation and aggregation on an endothelial surface with subsequent fibrin
furcation with normal intraluminal B-mode echogenicity after surgery.
mann et al. 2002, Steiner-Böckeretal.2004).Unfortunately, none of the large intravenous thrombolysis trials
have evaluated the presence of vessel occlusion or floating
thrombus before therapy, although aiming for recanalization of occluded arteries. The second therapeutic approach
applied in our patient is the emergency carotid endarterectomy (CEA). However, compared with standard carotid
surgery this procedure seems to carry a higher perioperative risk and morbidity, particularly in the neurologically
unstable patient (Buchan et al. 1988, Combe et al. 1990). It
should therefore only be considered in selected cases. A
noninvasive bedside evaluation of the brain-supplying
arteries may help to decide whether emergency CEA
would be appropriate. Finally, noninvasive medical treatment with anticoagulants (heparin, warfarin, or both) has
been reported in single cases or small series of patients,
but overall numbers are too small to allow controlled
comparison between the above approaches.
deposition. A straightforward hypothesis could be that
thrombocytosis leads to thrombus formation, but the correlation between high platelet counts and thrombosis is
poor (Kessler et al. 1982). Abnormal platelet activation and
function are probably more important than the absolute
platelet count. Anemia leads to increased flow velocities
and subsequent turbulent blood flow which may damage
the endothelium and lead to platelet aggregation. This
effect would be most prominent at vessel bifurcations
such as at the carotid sinus.
No guidelines have been published regarding the therapeutic management of floating carotid plaque material or
thrombi, and reported approaches are controversial. In our
patient, thrombolytic therapy was contraindicated despite
her arrival within the 3-hour time window because of her
underlying hematologic disease. In addition, thrombolysis
of a free-floating thrombus may increasethe risk of further
fragmentation, which could lead to embolization. In isolated studies, systemic thrombolysis was reported to be
effective in resolving acute carotid stent thrombosis (Ha-
Angiologic and Anatomic Aspects
Thrombus formation within the carotid artery classically
occurs if severe atherosclerotic disease is present. The
majority of carotid thrombi develop on stenotic or ulcerated atherosclerotic lesions (Caplan et al. 1984, Pessin et al.
1986). They may subsequently lead to vessel occlusion,
thromboembolic events, or both.
The true incidence of carotid thrombi is unknown.
Although artery-to-artery emboli from atherosclerotic
carotid artery lesions are a common cause of stroke, an
angiographic identification of a fixed or mobile carotid
thrombus is uncommon. In an analysis of about 2000
angiograms in patients with cerebral ischemia, thrombi
were only reported in 29 subjects (Buchan et al. 1988). In
cases with no atherosclerosis, thrombi have been associated with iron deficiency anemia, the use of illicit drugs,
and different types of blood hypercoagulability (Akins et
al. 1996, Konzen et al. 1995).
Discussion
137
A free-floating carotid thrombus seems to be a rare
phenomenon, perhaps as it is rarely recognized before
embolization. In addition, MRA and computed tomograph
angiography (CTA)—today often used as first-linediagnostic methods—currently provide only a snapshot image of
the thrombus and cannot displaythe floating character of a
thrombus, i. e., the change in its position over time. As
cerebral angiography is no longer a routine first-line diagnostic technique in ischemic stroke, carotid duplex sonography is currently the best method to demonstrate dynamic changes of vessel walls and their related structures
(Arning and Herrmann 1988). The presented case is an
excellent example, clearly demonstrating the floating
character of the thrombus with its characteristic oscillating movements. DSA was not required as no additional
information would have been gained, whereas catheter
angiography increases the risk of dislodgment of the
thrombus. This underlines the importance of performing
ultrasound in the early, hyperacute phase of stroke.
MRI is currently the optimal method to detect fresh
cerebral ischemic lesions. However, its ability to image
intravascular thrombi has so far not been well investigated. Our case report illustrates the potential pitfalls us-
ing the contrast-enhanced MRA. For initial calculation of
the image the widely used maximum intensity projection
(MIP) technique was used for post-processing of data. This
method only uses the image points with the maximal
intensity for image generation and therefore carries the
risk of incomplete thrombus visualization. Thus, source
data review is mandatory when assessing contrast-enhanced MRA. This likewise applies to CTA, in which MIP
is also used for data post-processing. However,here source
data evaluation is already established as all high-resolution cross-sectional images are analyzed on a regular basis.
Currently, dynamic information concerning potential
thrombus movement is not provided. However, the 360°
circumference of the thrombus can be depicted, and allows identification, for example, of apical thrombus segments without vessel wall adhesion, likely to be of floating
character. Our case underlines that knowledge of the vascularstatus,forexample,derivedfromaneurosonologic
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).
Degree of Neurosonologic Difficulty: Low
138
Case 3
Common Carotid Artery Occlusion
Clinical Presentation
A 64-year-old man was admitted with a transient rightsided facial paresis that had lasted a few minutes. At the
same time he experienced some slurring of his speech as
well as difficulty finding appropriate words. The symptoms started while he was standing in his kitchen, preparing breakfast. Six years previously, he had an ischemic
brain infarction with right-sided hemiparesis. An arteryto-artery embolism was suspected due to symptomatic
internal carotid artery (ICA) stenosis, and carotid endarterectomy 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) 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 magnetic resonance imaging (MRI) showed old
ischemic brain lesions in the left middle cerebral artery
(MCA) and anterior cerebral artery (ACA) territory, the left
central region, and in front of the left lateral ventricle. In
addition, multiple small focal lesions were found in the
right hemisphere. However, there were no signs of acute
cerebral ischemia in the diffusion-weighted MR images.
The cervical contrast-enhanced magnetic resonance angiogram showed no signals in the left common carotid
artery (CCA), internal carotid artery (ICA), and external
carotid artery (ECA). Regular signal intensities were
present within the right carotid arteries and the vertebral
arteries (VAs) (Figs. B3.1, B3.2).
Suspected Diagnosis
Left hemispheric transient ischaemic attack (TIA) of hemodynamic origin.
Questions to Answer by Ultrasound Techniques
• Was there evidence of occlusion or near occlusion of the
left CCA?
• Ifso,wasthereevidenceofcollateralbloodflowviathe
anterior communicating artery (ACoA) and posterior
communicating artery (PCoA) or leptomeningeal vessels
via the posterior cerebral artery (PCA)?
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 common, internal, and external carotid arteries.
The lumen of the left CCA was small and completely filled
with moderate hyperechogenic material, consistent with
an old occlusion. Assessment of the VAs was normal
(Figs.B3.3–B3.5).
Transcranial Duplex Sonography
A poststenotic flow pattern was seen in the left M1 segment of the middle cerebral artery (M1-MCA) with a positive oscillation effect following oscillation of the contralateral ICA at submandibular level. No flow signal was seen
in the intracranial segment of the left distal ICA. The left A1
segment of theanterior cerebralartery (ACA) flowdirection
was retrograde due to cross-flow from the contralateral
ICA. Inprojection of the ACoA (depth: 72 mm) an increased
flow velocity and turbulence was detected, indicative of a
functional stenosis. Flow in the right A1-ACA segment was
slightly increased (flow velocity: 135/65cm/s) but nonturbulent. Comparing both P1- and P2-PCA segments, a
mild increased flow velocity was seen on the left side. The
left ophthalmic artery (OA) could not be detected on the
transorbital approach (Figs. B3.6–B3.12).
Clinical Course
139
Conclusion
Extracranial occlusion of the left common, internal, and
external carotid arteries. Intracranial collateral blood flow
into the left MCA territory via ACoA and retrograde left A1ACA flow and probably via leptomeningeal collaterals of
the PCA.
Figures B3.13 and B3.14 show schematic drawings of the
extra- and intracranial brain-supplying arteries of a normal subject and of the patient.
Clinical Course
The acute clinical symptoms in our patient suggested a TIA
in the left cerebral hemisphere. Neurosonologic findings
confirmed the old left CCA occlusion which excluded an
embolic event and argued in favor of a hemodynamic
event; 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, “Parameters of Cerebral
Hemodynamics,” p. 60) was performed. MCA flow after
intravenous administration of 1 g acetazolamide led to a
Degree of Neurosonologic Difficulty: Low
Fig. B3.1 MR FLAIR image, axial plane. Old MCA infarction in the left
central region (arrow).
Fig. B3.3 Extracranial duplex, longitudinal plane. Mild increase of
flow velocity in the right CCA (flow velocity: 128/33 cm/s).
Fig. B3.2 Extracranial contrast-enhanced 3D MRA, coronal MIP. No
signals in the left common, internal, and external carotid arteries.
Fig. B3.4 Extracranial duplex, longitudinal plane (B-mode image):
The narrowed lumen of the left CCA is completely filled with moderate echogenic material (arrows).
Case 3 Common Carotid Artery Occlusion
140
Degree of Neurosonologic Difficulty: Low
Fig. B3.5 Extracranial duplex, longitudinal plane. Doppler spectrum
analysis shows a “stump-signal,” consistent with an occlusion. Note
the preserved flow signal of the internal jugular vein above the CCA.
Fig. B3.7 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow signal in the right M1-MCA in a depth
of 103 mm (flow velocity: 92/37 cm/s). Note the insonation was
performed from the contralateral side.
Fig. B3.6 TCCS (transtemporal approach), left-sided insonation,
midbrain plane: Mild poststenotic flow pattern in the left M1-MCA
with relative increase of the diastolic blood flow (flow velocity: 70/
34 cm/s).
Fig. B3.8 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Reversed flow direction in the left A1-ACA with
mild turbulence caused by the cross-flow via theACoA (flow velocity:
85/30 cm/s).
Fig. B3.9 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Raised but nonturbulent flow in the right A1-ACA
(flow velocity: 135/65 cm/s).
Fig. B3.10 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased flow velocity with turbulence, indicating
a functional stenosis of the ACoA (flow velocity: 150/80 cm/s).
23.4 % increase in flow velocity in the right MCA and 10.2%
in the left MCA. As a result of these findings and in the
absence of recent cerebral ischemia on MRI, it was decided
to keep the patient under regular review and make no
changes to his medication. He remained stable with no
further ischemic attacks over a follow-up period of 4 years.
Final Diagnosis
Final Diagnosis
Hemodynamic TIA in the left MCA territory caused by an
old CCA occlusion.
141
Degree of Neurosonologic Difficulty: Low
Fig. B3.11 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Mild increase of flow velocity in the left P1-PCA
(flow velocity: 97/40 cm/s).
Fig. B3.12 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow signalin theright P1-PCA (flowvelocity:
83/35 cm/s). . Note the insonation was performed from the contralateral side.
Fig. B3.13 Schematic drawing of the extra- and intracranial brainsupplying arteries. Red: Right-sided anterior circulation. Blue: Leftsided anterior circulation. Green: Posterior circulation. Pink: ACoA
andPCoA.1=ACoA;2=A2-ACA;3=A1-ACA;4=earlytemporal
M1-MCAbranch;5=M1-MCA;6=PCoA;7=P1-PCA;8=P2-PCA;
9=ICA;10=ECA;11=CCA;12=lenticulostriate arteries; 13=M2MCA;14=OA;15= SCA; 16=AICA;17= BA; 18=PICA;19=V4-VA;
20 = V3-VA; 21 = V 2-VA; 22 = SA.
Fig. B3.14 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 3. Note the occlusion of the
left common, internal, and external carotid arteries (circle). Blood
supply of the left MCA and ACA territory is via the ACoA. Additional
leptomeningeal collateralization of the left MCA territory via the left
PCA (green arrow).
Case 3 Common Carotid Artery Occlusion
142
Discussion
Clinical Aspects
Here we discuss the case of a 64-year-old patient with a
left CCA occlusion. Six years prior to presentation he
underwent CEA because of a symptomatic left ICA stenosis.
Some weeks after the intervention a complete left CCA
occlusion was noted which remained asymptomatic until
now, when he presented with a left hemispheric TIA.
CCA occlusions are fairly rare. In a stroke population an
incidence of about 2 % can be found (Hass et al. 1968, Riles
Degree of Neurosonologic Difficulty: Low
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 deficits (Podore et al. 1981). A small case series
reported orthostasis-related clinical symptoms in twothirds of 17 patients. TIAs were reported in 82 % of cases.
Completed stroke occurred in 59 % of patients (Levine and
Welch 1989).
The etiology of CCA occlusions is mostly atherosclerotic
in Caucasians, but other causes have to be considered. In a
series of 44 Asian patients, Takayasu arteritis was found in
25 % of cases, post-radiation angiopathy in 16 % of cases,
and cardioembolic events in 14% of cases (Tsai et al. 2005).
The prevalence of Takayasu arteritis is particularly high
within the Asian population. Furthermore, the occurrence
of nasopharyngeal carcinomas and their subsequent treatment with radiation therapy of the neck are more frequent
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 re-stenosis (< 18 months) occurred in
7.6–11.4 % of cases, whereas a late restenosis (18–60
months) after operationwas observed in 1.9–4.9 % of cases.
Notably, in this study no specific risk factor, especially the
continued use of tobacco or status of 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 of the ICA (Steinke et
al. 1991).
CCA occlusions can be divided into two types: the complete occlusion of CCA and ICA (type I) and the more
frequent isolated CCA occlusion (type II). As the ICA lumen
in the latter remains open, collateral blood flow into the
ICA can occur via extracranial branches through the retrograde external carotid artery (ECA). Ischemic events occur
more frequently in the combined CCA/ICA—type I occlusion, which suggests a hemodynamic etiology (Gerlock et
al. 1988, Tsai et al. 2005). Cerebral ischemia in type II
occlusions can also be caused by artery-to-artery embo-
lism, for example, from the vessel stump or from ECA
plaques(Barnettetal.1978).
Data regarding treatment strategies are scarce and heterogeneous. A surgical reopening is not attempted. Instead, in cases of severely impaired cerebrovascular reactivity due to insufficient collaterals and reoccurring hemodynamic 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,
p. 297).
Angiologic and Anatomic Aspects
Diagnosis and classification 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 wallchanges are present in the extracranial arteries,
and the thrombus itself is hyperechogenic or of heterogeneous echogenicity, an atherosclerotic cause is very likely.
In cases of cardioembolic occlusions or in situ thrombosis,
the thrombotic material appears hypoechogenic and may
even present floating parts (Tsai et al. 2005).
Intracranial compensation of a CCA occlusion (i. e. for the
ipsilateral ACA and MCA territory) requires competent and
effective collateral pathways, similar to the ICA occlusion.
The quality of the collateral pathways finally determines
theextentandseverityofthebraindamage.Thisisespecially true if an acute occlusion occurs. Transcranial ultrasound permits excellent opportunities to evaluate all potentialcollateralpathways.Inthepresentedcase,atypical
collateral pattern of a CCA occlusion 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 cross-flow was
easily depicted because of the excellent acustic temporal
bone window. A cross-flow was also assured by the applied submandibular oscillation of the contralateral ICA
which leads to typical flow transients on the MCA of the
occluded side. This oscillation test may be of help in patients with limited insonation quality to asses the collateralization pattern. The slightly increased flow within the
right CCA (contralateral to the side of the occlusion) indicates the intracranial cross-flow during extracranial ultrasound examination. Intracranially, bilateral comparison
of the P1- and P2-PCA segments demonstrates a slight leftsided flow increase, indicating additional leptomeningeal
collateralization via the PCA territory (see also Chapter 5,
“Stenoses and Occlusions,” p. 81, and “Collateral Pathways,” p.101).
Case 4
Temporal Arteriovenous Malformation
143
Clinical Presentation
A 45-year-old man presented with recurrent episodes of
impaired consciousness followed by a confusional state
lasting for several minutes. On admission to our hospital
his neurological examination was normal.
Initial Neuroradiologic Findings
Cerebral magnetic resonance imaging (MRI) showed a
lesion (30 ×25 mm) with numerous flow voids in the left
temporal region, extending temporo-mesially and showing intense enhancement on post-gadolinium 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). Magnetic resonance 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
• Detection of the feeding arteries.
• Detection and identification of the draining veins.
artery (PCA). Clear identification of the terminal ICA and
the proximal MCA was not possible. An arterial vessel
signal away from the probe with turbulent flow, increased
flow velocity, and reduced PI related to the vessel conglomerate was though to represent a major feeder originating from the distal ICA or proximal M1-MCA segment
(flow velocity: 155/84cm/s). More posteriorly, a similar
feeder signal with a marked turbulent flow and musical
murmurs toward the probe and a reduced PI was found in
the projection of the left proximal P2-PCA segment (flow
velocity: 150/78 cm/s). The distal left M1-MCA segment as
well as the left distal P2- and P3-PCA segments were
normal. Raised flow velocities with an increased PI were
observed in the enlarged left basal vein of Rosenthal (flow
velocity: 52/30 cm/s) but not in the contralateral corresponding vein (flow velocity: 13/10cm/s). Duplex sonographic measurement of the global cerebral circulation
time between the left ICA and the left IJV after intravenous
administration of an echo-contrast agent (Levovist) was
significantly shortened (3.4 s) compared with the normal
value of 7 ±1.3 s (Figs. B4.4–B4.11). (For further discussion
on this method, see Chapter 3, “Parameters of Cerebral
Hemodynamics,” p. 60)
Conclusion
Large left temporal AVM. Blood supply via feeding arteries
from the left distal ICA or proximal M1-MCA segment and
left proximal P2-PCA segment. Main drainage via the left
basal vein of Rosenthal.Significant shortening of the global
cerebral circulation time.
Initial Neurosonologic Findings
Extracranial Duplex Sonography
Comparison of the right and left sides revealed increased
flow velocity in the left internal carotid artery (ICA) and
reducedpulsatility(flowvelocity/PI:leftICA:81/48cm/s/
0.6, right ICA: 59/24 cm/s/ 0.95). Assessment of both vertebral arteries (VAs) was normal (Figs. B4.2, B4.3).
Transcranial Duplex Sonography
Color-mode imaging revealed atypical flow signals of multiple vessels (25 ×25 mm) between the main stem of the
left middle cerebral artery (MCA) and posterior cerebral
Conventional Angiography
Digital subtraction angiography (DSA) was performed
which confirmed 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. Extensive filling 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 (Figs. B4.12–B4.14).
Case 4 Temporal Arteriovenous Malformation
144
Clinical Course
Because of the reported recurrent complex-partial seizures, anticonvulsive therapy with carbamazepine 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 thelarge size of
the AVM. Partial embolization was considered to be pos-
Degree of Neurosonologic Difficulty: Low
sible via the endovascular approach, however, the patient
decided against any intervention. Repeated clinical and
ultrasound follow-up over an observational period of 4
years showed no further changes. No further seizures
have occurred to date.
Final Diagnosis
Symptomatic epilepsy with complex-partial seizures
caused by a left temporal AVM.
Fig. B4.1 MR T2-weighted image, axial plane. Multiple flow-voids in
the left temporallobe. Note the enlarged basal vein of Rosenthal as a
major AVM draining vein (arrowhead).
Fig. B4.3 Extracranial duplex, longitudinal plane. Right ICA with
normal flow and pulsatility (flow velocity: 59/24 cm/s, PI: 0.95).
Fig. B4.2 Extracranial duplex, longitudinal plane.Left ICA with slight
flow velocity increase and reduced pulsatility in comparison to the
contralateral side (flow velocity: 81/48 cm/s, PI: 0.6).
Fig. B4.4 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. AVM nidus in the left temporal lobe reflected by
the multicolored signals indicating different flow directions (arrowhead). Note the course of the M1-MCA (arrows) as well as the A1ACA (arrow).
Final Diagnosis
145
Degree of Neurosonologic Difficulty: Low
Fig. B4.5 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. The AVM nidus (arrowhead) appears larger in the
thalamic plane and the draining basal vein of Rosenthal becomes
visible (arrow).
Fig. B4.7 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow signal in the distal left M1-MCA (flow
velocity: 109/40 cm/s, normal PI).
Fig. B4.6 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased velocity and turbulent flow away from
the probe in projection of the terminal ICA or proximal MCA corresponding to an AVM feeder (flow velocity: 155/84 cm/s, reduced PI).
Fig. B4.8 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased flow velocity in the proximal left P2-PCA
toward the probe corresponding to an AVM feeder (flow velocity:
150/78 cm/s, reduced PI).
Fig. B4.9 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Normal flow velocity in the distal left P2-PCA (flow
velocity: 66/29 cm/s). Note the hidden flow signal of the basal vein of
Rosenthal within the spectrum of the PCA.
Fig. B4.10 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Left basal vein of Rosenthal with increased flow
velocity and “arterialized” flow signal (flow velocity: 52/33 cm/s,
increased PI)