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Case 29 Cerebral Venous Thrombosis
336
and/or CTA findings. A lack of contrast filling in the veins or
sinuses is the main diagnostic sign. Difficulties may be
encountered because of the great variability of venous
anatomy. The ability of digital subtraction angiography
(DSA) to assess dynamic aspects such as the delayed emptying of venous vessels and to detect collateral venous
pathways further increases its diagnostic sensitivity. However, the invasiveness of DSA limits its use in clinical daily
practice.
MR techniques have currently replaced DSA in most
institutions. MRI not only allows evaluation of parenchymal lesions but also direct visualization of the thrombus
itself. Considering the signal intensities in the T1- and T2-
Degree of Neurosonologic Difficulty: High
weighted images, MRI is able to assess the age of a thrombus over time. FLAIR images, however, should be interpreted cautiously. In low-flow vessels, for example, the
nondominant TS, a high signal intensity instead of a flow
void may appear, leading to the false-positive diagnosis of
CVT (Klingebiel et al. 2007).
Similar to DSA, TOF MRA is able to detect filling defects
in veins and sinuses. Because of its flow dependency, however, venous vessels with low flow velocities or an alternating flow may not be visualized. Again of major concern
are cases in which a nondominant TS is not visualized and
which may be confounded with thrombotic occlusion. As a
left-sided dominance of the TS is found in only about 25 %
of cases, the question of thrombosisoften rises with regard
to the left sinus (Ayanzen et al. 2000). Contrast-enhanced
MRA is more reliable and sensitive in the assessment of
normal and obstructed venous vessels but should also take
into account physiologic and anatomic differences between the right and left TSs (Farb et al. 2003, Klingebiel
et al. 2007).
MRI has also been performed to study recanalization
and its influence on clinical outcome. Follow-up TOF
MRA in 33 patients demonstrated that recanalization occurs within the first 4 months but not thereafter.ThrombosesoftheSSSreopenedinalmostallcases(98%)while42%
of TS thromboses remained occluded (Baumgartner et al.
2003). Similar results were referred in 37 patients, studied
by Stolz and co-workers. Most complete vessel normalization already occurred during the patient hospital stay
(41%). After 6 months a complete recanalization had occurred in 51 %. 19% demonstrated a partial recanalization
and in 30 % the occlusion remained. A late recanalization
between 6 and 12 months was observed in only one patient. Notably, the recanalization pattern was not correlated with clinical outcome (Stolz et al. 2004).
Unenhanced CT can be of diagnostic value. In severely
affected patients, a focal or generalized brain edema or
typical parenchymal bleeds may be present and can be
indirectly suggestive of venous congestion. Direct thrombus visualization, comparable to the dense media sign in
MCA occlusion, can be found within any vein or sinus,
depending on its location and extension, as was the case
in our patient (Goldberg et al. 1986). If contrast agents are
used, the “empty delta sign” canbefoundinSSSthrom-
bosis. The thrombus itself is spared but contrast enhancementisseeninthevesselwallsurroundingthethrombus.
CTA depicts venous vessels in healthy subjects as well as
venous pathology in patients with CVT (Klingebiel et al.
2002, Majoie et al. 2004). Its main advantage is the speed
of the procedure and its major flow independence, which
probable lowers the risk of false-positive findings in low
flow venous vessels. In two comparative studies with MR
techniques CTA was shown to be equivalent, however,
cortical vein thrombosis was not considered (Khandelwal
et al. 2006, Linn et al. 2007). As in all present techniques,
variations in the intracranial venous anatomy and properties of venous hemodynamics have to be taken into account to avoid false-positive interpretations.
Ultrasound has also been used to investigate patients
with CVT. Direct thrombus visualization is not possible but
similar to its use in deep venous thrombosis of the legs,
collateral pathways can be assessed and monitored (Stolz
et al.2002a, Valdueza et al.1999). Because of the absence of
valves in the intracranial venous system, flow may follow
the direction of need and any vein might serve as a collateral vessel. The size of the vessel, its ability to dilate, and
the extent of total collateral flow determine whether or
not an increase in velocity occurs, which can subsequently
be detected by ultrasound. TCCS has clear advantages over
the TCD approach due to its better anatomic orientation.
(for further discussion on venous anatomy and TCCS examination of intracranial veins and sinuses, see also Chapter 2, “General Venous Anatomy,” p. 40, and “Special Venous Anatomy and Ultrasound Anatomy,” p. 43). Different
collateral drainage patterns can be observed in CVT, depending on the location of the thrombus.
Superior Sagittal Sinus Occlusion
An interruption of flow in the SSS may be compensated for
by major collateral veins on the lateral surface of the brain,
which are effectively connected to one another and with
the principal venous outlets. Depending on the site of the
occlusion and the preexisting venous anatomy, venous
blood is collected by sylvian veins draining into the SphS
and cavernous sinus (CS), or by the vein of Labbé draining
totheTS.Thebloodmayalsoruntotheinternalcerebral
vein (ICV) and the BVR through transcerebral anastomoses.
Deep Cerebral Venous System Occlusion
In occlusion of the vein of Galen or the straight sinus (StS),
the BVR becomes an important collateral vessel with flow
reversal and blood distribution into two main pathways:
via the lateral mesencephalic vein to the petrosal vein and
superior petrosal sinus, and through the DMCV to the
sylvian veins, the SphS, and CS. The blood may also run
to the SSS through transcerebral anastomoses, which connect the deep cerebral venous system with the superficial
veins.
Discussion
337
Lateral Sinuses (Transverse and Sigmoid Sinus)
Occlusion
Variations of the lateral sinuses are common and of great
importance in understanding hemodynamic changes in
CVT. Acomplete separation between the SSS and StS drainageispresentinabout10%.Ifthisisthecase,aTSocclusion
may either lead to symptoms of StS or SSS occlusion. If only
the SiS is affected, flow in the ipsilateral TS will be reversed, caused by inflow from the vein of Labbé and other
vessels merging into the TS.
Based on the above collateral pathways, five ultrasound
constellations can be differentiated which can be found
alone or in combination in about 70 % of CVT patients.
Absent Flow Signals
Because of the known anatomic variation of intracranial
venous vessels an absent flow signal might either represent hypoplasia or aplasia or indicate thrombosis. In TS
thrombosis severalauthors have found that absent flow on
TCCS does not correlate well with a vessel occlusion. Unenhanced as well as echo contrast-enhanced TCCS has
frequently failed to detect aplasia, hypoplasia, and even a
patent TS (Baumgartner et al. 1997b, Delcker et al. 1999,
Ries et al.1997). Serial TCCS measurements, however, are
able to detect TS recanalization. Transient raised flow velocities may indicate venous stenosis during gradual recanalization (Stolz et al. 1999a).
Pathologic Differences between the Right and
Left Sides
In healthy subjects, bilateral differences > 50 % are usually
not observed in the paired BVR and DMCV. In CVT they
often persist even over longer periods of time and might
indicate partial recanalization. InTS thrombosis a compensatory increase in flow in the contralateral TS can frequently be observed (Stolz et al. 1999a, 2002a). As only
in about 25 % of cases symmetric TSs are present, asymmetric flow velocities within the TS should be considered
carefully.
Increased Flow Velocities
Raised flow velocities in venous collaterals are the most
frequent finding in CVT. If detected, they are highly suspicious of an underlying CVT. A variety of pitfalls, however,
have to be considered. Increased flow velocities may be
detected in the inflow and outflow region of the CS. If
present, they do not reflect venous pathology but are
rather caused by physiologic venous anatomic narrowing
attheentranceandexitoftheCS.Physiologicallyraised
flowcanalsobeobservedintheproximalStSoreveninthe
TS, for example, if large pacchionian granulations cause
venous vessel narrowing. Also, increased velocities may be
detected in partially recanalized sinuses. Raised venous
velocities may finally be observed in arteriovenous malformations (AVMs) or dural fistulas (Harrer et al. 2005) and
in generalized or local hyperemia. The latter can be observed in herpes simplex virus (HSV) encephalitis (Doepp
et al. 2006).
Reversed Venous Flow Direction
A reversed BVR flow is a frequent finding in StS occlusion
(Baumgartner et al. 1997b, Stolz et al.2002a, Valdueza et al.
1999). In these cases the BVR mainly serves as a collateral
for blood deriving from the inferior sagittal sinus, vein of
Galen, and ICV, draining into the SphS or CS. Occasionally,
retrograde flow can also be detected in the proximal part
of a distally thrombosed transverse sinus (Stolz et al.
2002a).
Venous High Intensity Signals
Venous high intensity signals can be observed in the outflow vessels of patients with CVT. They are thought to be
related to the fragmentation of proximally located thrombotic material. Their clinical significance is yet unclear
(Valdueza et al. 1997).
In about 30 % of cases with CVT, no pathologic sonographic
signs can be detected. Therefore, normal TCD and/or TCCS
do not allow excluding a CVT. Ultrasound cannot replace
CTA or MRA as primary diagnostic tool, but may be used as
a screening method. It may give further insights into the
disturbed intracranial venous circulation and may help in
assessing prognosis if serial measurements are performed
in patients with altered venous flow signals. High initial
venous flow velocities correlate with altered consciousness (Valdueza et al. 1999) while patients with initially
normal venous flow signals or flow normalization within
90 days demonstrate a significantly better clinical outcome (Stolz et al. 2002a).
Degree of Neurosonologic Difficulty: High
338
Case 30
Multilocular Extra- and Intracranial Stenoses and Occlusions
Clinical Presentation
A 41-year old woman presented to a district general hospital because of transient episodes of numbness in the left
face and hand as well as left-sided blurred vision. There
she underwent cerebral magnetic resonance imaging
(MRI) and MR angiography (MRA). She was subsequently
commenced on aspirin and 3 weeks later referred to our
department for further clinical evaluation. No ultrasound
examination was performed. The medical history revealed
migraine, and nicotine and alcohol misuse. There was no
known arterial hypertension and she did not take any
medication. On admission, her neurologic examination
was normal.
Initial Neuroradiologic Findings (Day 1)
Cerebral MRI on admission to the district general hospital
showed multiple signal abnormalities in the right hemisphere, consistent with internal border zone infarction
(BZI). Contrast-enhanced extracranial MRA revealed vessel wall irregularities in the carotid arteries and occlusion
of the left external carotid artery (ECA). Intracranially,
time-of-flight (TOF) MRA demonstrated absent flow signals in the left distal internal carotid artery (ICA) and the
right M1 middle cerebral artery (MCA), and A1 anterior
cerebral artery (ACA) segments. On T2-weighted images,
however, a signal void of the right M1-MCA segment was
clearly visible indicating patency of the MCA (Figs. B30.1–
B30.4).
Suspected Diagnosis
Recurrent left-sided sensory transient ischemic attacks
(TIAs) presumed to be of hemodynamic origin because of
suspected pathology of the right MCA. Asymptomatic left
distal ICA occlusion.
Questions to Answer by Ultrasound Techniques
• Was there evidence of a distal occlusion of the asymptomatic left intracranial ICA?
• Were there signs of atherosclerosis or vasculitis?
Initial Neurosonologic Findings (Day 20)
Extracranial Duplex Sonography
B-mode sonography revealed left-accentuated severe
atherosclerotic vascular changes with iso- to hyperechogenic plaques, especially in the carotid sinuses. No flow
signal was seen in the left external carotid artery (ECA).
Color-mode image of the left proximal ICA demonstrated a
lumen reduction of about 40–50 % caused by hypoechogenic material. The flow signal in this area was regular
(flow velocity: 115/58 cm/s). A markedly reduced flow
velocity was seen in the right ICA (flow velocity: 24/
11 cm/s). Assessment of the vertebral arteries (VAs) and
right ECA revealed normal findings (Figs. B30.5–B30.7).
Transcranial Duplex Sonography
Raised flow velocities were found in the left-sided carotid
siphon (flow velocity: 228/94 cm/s) and proximal M1MCA segment (flow velocity: 221/131cm/s). The distal
MCA segments on the left side revealed a mild poststenotic
flow pattern. A marked, slightly turbulent and poststenotic
flow pattern was seen in the left A1-ACA segment which
seemed to supply both A2 segments (flow velocity: 132/
69 cm/s). The anterior communicating artery (ACoA) could
not be detected. The left posterior cerebral artery (PCA)
was almost normal with only slightly increased velocities.
The right proximal M1-MCA segment demonstrated a turbulent flow with increased velocity (flow velocity: 161/
74cm/s). The proximal M2 branches revealed a distinct
poststenotic flow pattern. No right A1-ACA segment was
detected. Raised flow velocities were found in the right P1and P2-PCA segments indicating leptomeningeal collateralization (flow velocity: 159/88 cm/s). No flow signal was
seen in the left ophthalmic artery (OA) while the right OA
flow was orthograde. Unsuspicious Doppler spectra were
seen within the VAs and the basilar artery (BA) (Figs.
B30.9–B30.15).
• Were there real occlusions of the right M1-MCA and A1ACA segments?
Follow-up Neurosonologic Findings (Day 29)
339
Conclusion
Severe atherosclerosis in the extracranial segments of the
brain-supplying arteries with a left-sided proximal ICA
stenosis of about 40–50% and left ECA occlusion. Intracranially, left-sided high-grade ICA siphon and proximal
M1-MCA stenoses. On the right side hemodynamically
relevant proximal M1-MCA stenosis and A1-ACA occlusion
or aplasia. Blood supply to the right MCA territory via the
ipsilateral ICA and leptomeningeal PCA anastomoses. Supply of the right ACA territory assumed to be via cross-flow
from the contralateral A1-ACA segment.
Conventional Angiography (Day 22)
DSA confirmed a left-sided moderate extracranial ICA
stenosis and occlusion of the ECA as well as a high-grade
left-sided intracranial ICA and moderate M1-MCA stenosis. Blood supply of both ACA territories was provided by
the left A1-ACA segment. On the right side the A1-ACA and
M1-MCA segments seemed to be occluded. During the late
arterial sequences of the right ICA projection, however, a
distinct temporal branch and a prominent insular M2
branch became visible. Abnormal dilated lenticulostriate
vessels corresponding to a vascular collateral network
were seen adjacent to the affected main vessels. Left VA
injection revealed a marked collateral flow to the right
MCA territory via leptomeningeal collaterals from the
right PCA. Finally, the intracranial vessel status was evaluated as a near occlusion of the right M1-MCA segment
with collateralization of the MCA territory via the right
PCA and right A1-ACA occlusion with collateralization via
the contralateral ACA (Figs. B30.16–B30.21).
Figure B30.22 shows a schematicdrawing of the extra- and
intracranial brain-supplying arteries of the patient at this
stage.
Clinical Course (1)
The multilocular extracranial and intracranial pathology
wasattributedtoatherosclerosisonthebasisoftheknown
severe nicotine and alcohol misuse and newly diagnosed
hypercholesterolemia and hyperhomocysteinaemia.
During the first few days in the hospital the patient had
further mild clinical events with sensory disturbances of
the left hand while her blood pressure was slightly elevated. Several days later she developed new recurrent
contralateral symptoms—a severe right-sided brachiofacial paresis and global aphasia—each lasting 20–30 minutes. She was then referred to the stroke unit for further
monitoring and blood pressure control. Despite a systolic
bloodpressureof200mmHgachievedbydopamineinfusion she finally developed severe akinetic mutism. Follow-up MRI 1 day later revealed a new left-sided internal
BZI, larger than on the right side. Extracranial contrastenhanced MRA and intracranial TOF MRA showed no signal in the left CCA, ICA, ECA, and ACA and a weak signal in
both MCAs (Figs. B30.23–B30.25).
Questions to Answer by Ultrasound Techniques
• Was there a real complete occlusion of the left carotid
arteries?
• What is the vessel status of the right side?
• Was there permanent near occlusion of the right M1-
MCA segment?
Follow-up Neurosonologic Findings
(Day 29)
Extracranial Duplex Sonography
The lumen of the left ICA and common carotid artery (CCA)
was still visible. The flow pattern of the left ICA had
changed revealing now a high resistance flow signal with
a low and short systolic flow and completely absent diastolic flow, suggestive of distal ICA occlusion below the OA
origin (Fig. B30.26). The left ECA signal remained absent.
Flow signals in the right carotid arteries and the VAs remained unchanged.
Transcranial Duplex Sonography
No flow signal was detected in the left distal ICA. The
turbulent flow pattern of the left MCA remained unchanged, however, flow velocities had decreased (flow
velocity: 81/46cm/s). Also the flow velocity of the left
A1-ACA segment was found to be lower than before and
the poststenotic flow patternhad becomemore prominent
if compared with the first ultrasound examination (flow
velocity: 53/33 cm/s). Raised flow velocities were now
found for the first time in the left P1-PCA segment (flow
velocity: 190/99cm/s). Distinct turbulences could be detected in the left posterior communicating artery (PCoA)
indicating collateral function and blood supply toward the
anterior circulation. Correspondingly, a raised flow velocity but no turbulent flow was now found in the BA (flow
velocity: 208/106 cm/s) (Figs. B30.27–B30.31). Unchanged
flow patterns were seen in the right MCA and OA.
Conclusion
Progressive vessel pathology with distal occlusion of the
left ICA and inadequate collateralization via the left PCoA.
Unchanged right-sided vessel status with near occlusion of
the M1-MCA segment.
Degree of Neurosonologic Difficulty: High
Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions
340
Clinical Course (2)
Considering the dynamic vascular process, intravenous
heparin, aiming for a twofold rise of partial thromboplastin time (PTT) was started. The new left distal ICA occlusion
was finally considered to be of atherosclerotic origin. Iatrogenic dissection of the ICA after conventional catheter
angiography was discussed, although the latency between
DSA and onset of symptoms was 4 days. Cervical MRI,
however, revealed no mural hematoma on cross-sectional
images. Biopsyof one branch of the STeA revealed no signs
of large vessel arteritis.
Degree of Neurosonologic Difficulty: High
The akinetic mutism improved slowly during the following days. Treatment was changed from heparin to antiplatelet therapy with clopidogrel. After clinical stabilization,
the patient was discharged for rehabilitation with mild
right-sided hemiparesis and motor aphasia. Follow-up
after 2 months revealed no further clinical events but
further regression of paresis and aphasia. CT scan ruled
out further infarction. CTA findings were compatible with
left M1-MCA stenosis and right M1-MCA near occlusion
(Fig. B30.32).
Follow-up Neurosonologic Findings (3 Months)
Extracranial Duplex Sonography
B-mode sonography showed hyperechogenic material occluding the left ICA, ECA,and distalCCA. Color-mode imag-
ing revealed absent color signal. Doppler spectrum analysis showed a stump signal in the proximal CCA (Fig.
B30.33).
Transcranial Duplex Sonography
The results were unchanged from the preceding examination (not shown).
Conclusion
Distal occlusion of the left-sided CCA due to retrograde
thrombosis. Blood supply of the left MCA territory and
both ACA territories from the posterior circulation via
the left PCoA. Unchanged near occlusion of the right M1MCA segment with blood supply from the ipsilateral ICA
and via leptomeningeal collaterals from the PCA.
Figure B30.34 shows a schematicdrawing of the extra- and
intracranial brain-supplying arteries of the patient.
Final Diagnosis
Marked atherosclerosis with right M1-MCA near occlusion
and left M1-MCA stenosis. Secondary left intracranial ICA
occlusion and subsequent ipsilateral retrograde CCA
thrombosis. Unfavorable collateralization via the circle of
Willis (CW) leading to bilateral internal BZIs.
Fig. B30.1 Cerebral MR T2-weighted image, axial plane. A rosarylike
pattern of deep whitematter signal abnormalities in the right corona
radiata, consistent with an internal border zone infarction (arrows).
(Courtesy of Dr. Grüger, Martin Gropius Krankenhaus, Eberswalde,
Germany.)
Fig. B30.2 Extracranial contrast-enhanced MRA, coronal MIP. Multiple vessel wall irregularities in the carotid arteries. Missing left ECA
signal and left proximal ICA stenosis (large arrowhead). Suspected
intracranial occlusion of the left ICA at the level of the carotid siphon
(singlearrow).Notetheabsentsignal of the right M1-MCA (arrows)
but presence of insular branches at the same time(small arrowhead).
(Courtesy of Dr. Grüger, Martin Gropius Krankenhaus, Eberswalde,
Germany.)
Final Diagnosis
341
Degree of Neurosonologic Difficulty: High
Fig. B30.3 Intracranial 3D TOF MRA, coronal MIP. Assumed occlu-
sion of the right M1-MCA and A1-ACA segments (small arrows).
Note a visualization of the most proximal parts of the M1-MCA and
A1-ACA (arrowheads). Note also the visualization of an insular MCA
branch (short arrow) and a temporal branch(large arrow). (Courtesy
of Dr. Grüger, Martin Gropius Krankenhaus, Eberswalde, Germany.)
Fig. B30.5 Extracranial duplex, longitudinal plane (color-mode image). Normal flow signal in the left ICA (flow velocity: 115/56 cm/s).
Note the prominent hypoechogenic plaque (arrows).
Fig. B30.4 Cerebral MR T2-weighted image, axial plane. Flow void in
the right M1-MCA segment indicating patency of the vessel (arrows). Compared to the left M1-MCA, the diameter appears reduced. (Courtesy of Dr. Grüger, Martin Gropius Krankenhaus, Ebers-
walde, Germany.)
Fig. B30.6 Extracranial duplex, transverse plane (color-mode image). Axial sectioning reveals a lumen reduction of the left proximal
ICA of about 40–50 % caused by hypoechogenic excentric plaque.
Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions
342
Degree of Neurosonologic Difficulty: High
Fig. B30.7 Extracranial duplex, longitudinal plane. A distinct re-
duced flow signal was seen in the right ICA (flow velocity: 24/
11 cm/s).
Fig. B30.9 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Stenotic flow pattern in the left proximal M1-MCA
(flow velocity: 221/131 cm/s).
Fig. B30.8 TCCS (transtemporal approach), left-sided insonation,
upper pontine plane. Stenotic flow pattern in the left carotid siphon
(flow velocity: 228/94 cm/s).
Fig. B30.10 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Mild poststenotic flow pattern in the distal left M1MCA (flow velocity: 65/25 cm/s).
Fig. B30.11 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Turbulent and slightly altered poststenotic flow
pattern in the left A1-ACA which seemed to supply both A2-ACAs
(flow velocity: 132/69 cm/s).
Fig. B30.12 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Color flow image of the circle of Willis with strong
left A1- and A2-ACAs and missing right A1-ACA (arrow). Note the
good color imaging of the right M1-MCA (arrowhead).
Final Diagnosis
343
Degree of Neurosonologic Difficulty: High
Fig. B30.13 TCCS (transtemporal approach),right-sided insonation,
midbrain plane. Stenotic flow pattern with increased and turbulent
flow in the right proximal M1-MCA (flow velocity: 161/74 cm/s).
Fig. B30.15 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Prominent flow in the right P1- and P2-PCA, indicating leptomeningeal collateralization. Here the P1-PCA is shown (flow
velocity: 159/88 cm/s).
Fig. B30.14 TCCS (transtemporalapproach), right-sidedinsonation,
thalamic plane. Severe poststenotic flow pattern in one right M2MCA branch (flow velocity: 58/33 cm/s).
Fig. B30.16 DSA, left CCA injection, posteroanterior view. Proximal
ICA stenosis of about 50 % (arrow).
Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions
344
Degree of Neurosonologic Difficulty: High
Fig. B30.17 DSA, right ICA injection, posteroanterior view, late ar-
terial phase. Visualization of a temporal branch at the ICA/MCA
junction (arrowhead) and a prominent insular M2-MCA branch (arrow). The M1-MCA and the A1-ACA segments were not visible. Note
also the fine network of lenticulostriate vessels (arrows).
Fig. B30.18 DSA, left ICA injection, posteroanterior view. Both ACA
territories are supplied via the left A1-ACA. Stenosis of the distal
carotid siphon (arrow) as well as of the proximal M1-MCA (arrowhead). Note also the early M1-MCA bifurcation on the left side.
Fig. B30.19 DSA, right VA injection, posteroanterior view. Collateral
leptomeningeal flow to the right MCA territory via the right PCA
(arrows).
Fig. B30.20 DSA, left and right CCA injection, posteroanterior view,
early arterial phase, superimposed image of left and right CCA
injection, facilitating comparison of the right and left vessel status.
Suspected right terminal ICA occlusion (arrow).
Final Diagnosis
345
Degree of Neurosonologic Difficulty: High
Fig. B30.21 DSA, left and right CCA injection, posteroanterior view,
left CCA injection: early arterial phase, right CCA injection: late
arterial phase, superimposed image of left and right CCA injection,
facilitating comparison of the right and left vessel status. Absent
filling of the right M1-MCA segment. However, despite the signal
gap, the presence of several insular branches (arrows) argued in
favor of a right M1-MCA patency.
Fig. B30.22 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 30 (initial findings). Near
occlusion of the right M1-MCA (circle) and missing A1-ACA. Leptomeningeal collateral blood flow tothe MCA territory from the right
PCA (green arrow). Perfusion of the right ACA territory via the
contralateral A1-ACA. Left extracranial mild ICA stenosis and ECA
occlusion (circles). Left intracranial ICA and M1-MCA stenosis
(circles).
Fig. B30.23 Cerebral MR FLAIR image, axial plane. More confluentlike pattern in the left corona radiata, consistent with a new contralateral internal border zone infarction.
Fig. B30.24 Extracranial contrast-enhanced MRA, coronal MIP.
Missing signal of the left CCA, ICA, and ECA. Note the prominent
signal of the left internal jugular vein (arrow).Unchanged findingson
the right side.