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299Discussion

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.

have focused on the diagnostic performance of bone subtraction CTA for intracranial aneurysm detection, as these tend to be located in close proximity to the skull base. There, the diagnostic accuracy for bone subtraction dual-source CTA was similar to that of DSA (the gold standard) (Cheng et al 2015, Lu et al 2012).

Contrast-enhanced (ce)-MRA and TOF-MRA are not limited by vessel calciﬁ cation. However, being a ﬂ ow-sensitive method 3D-TOF-MRA is susceptible to artifacts generated by the physiologic turbulent ﬂ ow with- in the carotid siphon, which might be ampliﬁ ed by ves- sel elongation, a feature frequently seen with increasing age. Therefore, bilateral signal interruptions within the carotid siphon are frequently found. In case of a real underlying stenosis, 3D-TOF-MRA tends to aggravate the grade of stenosis or even demonstrate complete occlusion. Consequently, for skull base vessel assessment, ce-3D-FLASH-MRA is superior to 3D-TOF-MR A despite venous enhancement of the cavernous sinus (Yang et al

2002). In the case presented here these artifacts were not of relevance as little elongation was present in our young patient and the clinical symptoms matched the side of the pathologic ﬁ nding. Therefore, a stenosis was beyond doubt. It was only the degree of stenosis that was questioned, as the conclusions of the various imaging methods were initially contradictory.

Interestingly, DSA—performed on the same day as the MRI—was unable to clearly conﬁ rm the MRA diagnosis. Despite imaging in four diﬀ erent projection planes, only a mild ICA stenosis could be suspected, which would

probably have been overlooked without knowledge of the MRA ﬁ ndings. Presumably the stenosis was somewhat masked in DSA by the overlying posterior communicating artery (PCoA) oﬀ shoot, which was less of a problem in TOF- MRA due to the lower ﬂ ow (and, correspondingly, size). Also, the MRA MIP is limited to a so-called slab or volume deﬁ ned by the operator, thus limiting the extent of overly- ing vessels in projection images. Last but not least, state-ofthe-art DSA nowadays includes rotational 3D angiography, allowing for 3D image reconstructions of unprecedented image quality, which were not available in our case and most probably would have revealed the critical stenosis.

Subsequently, the clear ultrasound ﬁ nding of a high-grade carotid siphon stenosis was surprising as it corrected the DSA interpretation and conﬁ rmed the MRA ﬁ nding. To date, DSA is considered to be the method providing the highest spatial resolution, correcting doubtful ﬁ ndings of the other methods almost without question. However, our example demonstrates that it is always valuable to combine the ﬁ nd- ings of the available diagnostic techniques to avoid potential misdiagnoses. The interpretation of ﬁ ndings should include critical assessment of the strengths and weaknesses of each method. A problem of standard biplane DSA technique is the limited number of imaging planes, often restricted to the “routine” lateral and posteroanterior views. However, this was not the underlying reason in our case. We assume that here the unique anatomy of the carotid siphons and the distribution of the diluted contrast agent within this vessel segment was the main factor (for further discussion on evaluation of intracranial stenoses, see Case 5).

300

Case 15

Near-occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

Clinical Presentation

A 58-year-old man was admitted after suﬀ ering a tran- sient left-sided weakness and confusion 3 hours before presentation. The symptoms had already completely resolved. The patient was a smoker and suﬀ ered from ar- terial hypertension, which had been treated for 15 years. The neurologic examination revealed no deﬁ cits.

Initial Neuroradiologic Findings

Cerebral MRI on the day of admission demonstrated a large anterior territorial infarction in the right middle cerebral artery (MCA) territory. Contrast-enhanced magnetic resonance angiography (ce-MRA) was consistent with a near-occlusion of the right internal carotid artery (ICA) with a marked poststenotic vessel collapse and a high-grade stenosis of the contralateral ICA. Intracranial time-of-ﬂ ight (TOF) MRA showed only a weak signal in the right ICA and right MCA corresponding to the extracranial ICA near-occlusion. A small ipsilateral posterior communicating artery (PCoA) was seen. The nevertheless weak MCA signal indicated a compromised collateral pathway. The lower signal intensity of the left M1-MCA, compared with the ipsilateral posterior cerebral artery (PCA), also indicated impaired left-sided perfusion (Fig. B15.1 and

Fig. B15.2).

Suspected Diagnosis

Right hemispheric transient ischemic attack (TIA) and large right MCA territorial infarction, probably caused by artery-to-artery embolism from right-sided near-occlusion of the ICA. Asymptomatic high-grade stenosis of the left ICA.

Questions to Answer by Ultrasound Techniques

• Could the right ICA near-occlusion and the left highgrade ICA stenosis be conﬁ rmed?

• What was the underlying vascular pathology?

• What was the resulting intracranial collateral ﬂ ow pattern?

Initial Neurosonologic Findings

Extracranial Duplex Sonography (Day 2)

B-mode imaging demonstrated bilateral atherosclerotic changes, predominantly with homogeneous hypoechoic plaques in both carotid bifurcations. There were no signs of arteritis. The right common carotid artery (CCA) displayed a mildly increased pulsatility. Both external carotid arteries (ECAs) had ﬂ ow signals considered to be “internalized.” The right ICA showed a stump signal at the bulb. However, after adjusting the settings for low ﬂ ow signals, i.e., reduced pulse repetition frequency (PRF) and increased gain, a severe turbulent ﬂ ow with a ﬂ ow velocity of 121/38 cm/s was detected slightly distal to the ICA bulb. Distal to that, the ICA was partly collapsed (diameter 3.1 mm) showing a marked poststenotic ﬂ ow pattern and low velocities (14/5 cm/s). The left ICA revealed a stenotic ﬂ ow signal with turbulence and a marked increased ﬂ ow velocity (394/231 cm/s). The distal vessel segments displayed a spiculated ﬂ ow sig- nal but otherwise no signs of a hemodynamic restriction. Normal ﬁ ndings were seen in the vertebral arteries (VAs) (Fig. B15.3–Fig. B15.11; see also Video

Transcranial Duplex Sonography

The right MCA and anterior cerebral artery (ACA) were antegrade perfused and presented a moderate poststenotic ﬂ ow pattern. A residual ﬂ ow was seen in the C6-ICA. The ophthalmic artery (OA) had a marked retrograde ﬂ ow (62/26 cm/s). Flow velocity in the right P1 segment of the PCA was higher than in the ipsilateral P2-PCA (79/35 cm/s versus 43/17 cm/s) indicating collateral ﬂ ow via the PCoA. Accordingly, the PCoA was detected with a mild turbulent ﬂ ow. On the left side, a more compromised anterior circulation was observed. The poststenotic ﬂ ow pattern of the antegrade perfused M1-MCA and A1-ACA was more obvious. The A1-ACA revealed a high velocity indicating collateral ﬂ ow (98/53 cm/s). The C6-ICA was markedly reduced in ﬂ ow and revealing a severe poststenotic ﬂ ow pat- tern. As on the right side, a marked retrograde ﬂ ow was seen in the OA. Unlike the right side, no PCoA was seen and the P1- and P2-PCA segments had continuously increased systolic ﬂ ow velocities ~80–90 cm/s, indicating

B15.1).

301Follow-up Neurosonologic Findings (3 Months)

leptomeningeal collateral ﬂ ow. Accordingly, elevated ﬂ ow velocities were seen in cortical PCA branches, the

anterior temporal artery (ATA), and occipitotemporal artery (OTA). Normal ﬂ ow patterns were seen in the vertebrobasilar arteries (Fig. B15.12–Fig. B15.27; see also Video

B15.2).

Conclusion

Bilateral severe atherosclerotic macroangiopathy with near-occlusion of the right ICA and high-grade stenosis (>80% according to NASCET criteria, >90% according to ECST). Collateral blood ﬂ ow to the right anterior circula- tion from the PCA via the PCoA and retrograde OA and to the left anterior circulation leptomeningeal via the ACA and PCA as well as via a retrograde OA.

Conventional Angiography (Day 3)

Because of the bilateral impaired anterior circulation perfusion we decided to treat the symptomatic right ICA by stenting without delay. Digital subtraction angiography (DSA) conﬁ rmed the near-occlusion of the right ICA. In the early arterial phase the ICA appeared occluded (similar to the initial duplex examination analyzing the carotid bulb). In the subsequent images (late arterial phase) the residual ﬂ ow and the collapsed vessel were detected. DSA also conﬁ rmed the left high-grade ICA stenosis (Fig. B15.28).

Fig. B15.29 shows a schematic of the patient’s extraand intracranial brain-supplying arteries before stenting of the right ICA.

and the PCA signals remained unchanged. The increased ﬂ ow velocity in the right A1-ACA was therefore assumed to indicate leptomeningeal collateral ﬂ ow to the left a n t e r i o r c i r c u l a t i o n ( Fig. B15.32, Fig. B15 .33, Fi g. B15.34,

Fig. B15.35, Fig. B15.36).

Conclusion

Right ICA after stent insertion without residual stenosis and normalized right intracranial circulation. Unchanged left high-grade ICA. The left collateral circulation ameliorated slightly via the activation of the right A1-ACA.

Fig. B15.37 shows a schematic of the extra- and intracranial brain-supplying arteries after successful stenting of the right ICA.

Clinical Course (2)

Because of the patient’s relatively young age and the hypoechoic plaques, considered to increase the risk of further strokes, a stent was also inserted in the left ICA 2 months later. Since then, the patient has had no further ischemic attacks. Neuropsychologic testing revealed a signiﬁ cant improvement of his cognitive function, especially of his alertness, response time, and capability of readjustment.

Follow-up Neuroradiologic Findings (2 Months)

Clinical Course (1)

The stenting proceeded uneventfully and the patient was started on aspirin and clopidogrel for 6 weeks. No ischemic events occurred. Notably, the patient and his wife reported that his neuropsychologic status, alertness, drive, and concentration had increased and had ameliorated even when compared with his status before stroke.

Follow-up Neurosonologic Findings (6 Weeks)

Extracranial Duplex Sonography

Doppler spectrum analysis showed a normalized ﬂ ow in the right stented ICA segment without evidence of restenosis. The left high-grade ICA stenosis remained unchanged (Fig. B15.30 and Fig. B15.31).

Transcranial Duplex Sonography

The right ICA, MCA, ACA, and PCA segments as well as the right OA demonstrated normalized ﬂ ow signals i n d i c a t i n g a d e q u a t e ﬂ ow and remission of the PCoA ac- tivation. Interestingly, ﬂ ow velocity of the right A1-ACA increased markedly. The left M1-MCA as well as A1-ACA

MRI showed no new ischemic or other lesion after the second intervention. TOF-MRA presented normalized ﬁ ndings with bright signals of both MCA and ACA now similar to the PCA signals. The right PCoA was no longer visible, indicating the abolished PCoA ﬂ ow (Fig. B15.38).

Follow-up Neurosonologic Findings (3 Months)

Extracranial Duplex Sonography

Doppler spectrum analysis within the left ICA stent showed a normalized ﬂ ow, and the pulsatility index (PI) of the left ECA had increased. The contralateral carotid artery remained unchanged (not shown).

Transcranial Duplex Sonography

Intracranial ﬁ ndings in the left ICA, MCA, ACA, PCA, and OA had normalized. Interestingly, ﬂ ow velocities in the right C6-ICA and A1-ACA were lower than before, indicating the disappearance of the previous leptomeningeal collateral ﬂ ow from the right A1-ACA to the left anterior circulation. Also, the proximal cortical branches of the left PCA (ATA and OTA) were no longer detected (Fig. B15.39–

Fig. B15.47).

302 Case 15 Near-Occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

Fig. B15.1 (A) MR diﬀ usion-weighted image, axial plane. Large, right-sided anterior territorial MCA infarction mostly sparing the basal ganglia and internal capsule. (B) Ce-MRA, left anterior oblique MIP. Signal gap in the right proximal ICA (arrow) and collapsed vessel up to the carotid siphon (small arrows) compatible with a near-occlusion. The left ICA shows a small signal gap (arrowhead) without distal vessel collapse (small arrowheads).

CCA-R

Fig. B15.3 Extracranial duplex, longitudinal plane. Doppler spectrum analysis revealed only a mild resistance ﬂ ow signal in the right CCA (ﬂ ow velocity 101/23 cm/s, PI = 1.6).

Fig. B15.2 Intracranial 3D TOF-MRA, axial MIP. Markedly reduced signal in the right A1-ACA and M1-MCA (small arrows). Note the right PCoA (arrow). The left A1-ACA and M1-MCA (arrowhead) presented a less reduced signal intensity compared with the right side but were also clearly aﬀ ected if compared with the two bright PCA signals.

ECA-R

Fig. B15.4 Extracranial duplex, longitudinal plane. Right ECA shows a mildly increased diastolic, i.e., “internalized” blood ﬂ ow signal (ﬂ ow velocity: 128/29 cm/s, PI = 1.8).

ICA-R

Fig. B15.5 Extracranial duplex, longitudinal plane. Right ICA showing a stump signal in the bulb, suggestive of ICA occlusion.

ICA-R

Fig. B15.6 Extracranial duplex, longitudinal plane. Slightly more distal and after adjusting PRF to visualize low ﬂ ow signals a stenotic ﬂ ow signal with marked turbulence but not really high velocities can be detected in the right proximal ICA (ﬂ ow velocity 121/38 cm/s).

303Follow-up Neurosonologic Findings (3 Months)

ICA-R

Fig. B15.7 Extracranial duplex, longitudinal plane. Right midpart ICA showing a severe poststenotic ﬂ ow pattern with reduced ﬂ ow veloc- ities (14/5 cm/s) in an almost collapsed vessel (diameter 3.1 mm).

ECA-L

CCA-L

Fig. B15.8 Extracranial duplex, longitudinal plane. Left CCA Doppler spectrum without any relevant prestenotic ﬂ ow pattern (ﬂ ow velocity 126/38 cm/s, PI = 1.3).

ICA-L

Fig. B15.9 Extracranial duplex, longitudinal plane. Left ECA shows a mildly increased diastolic, i.e., “internalized” blood ﬂ ow signal (ﬂ ow velocity 175/52 cm/s, PI = 1.5).

ICA-L

Fig. B15.11 Extracranial duplex, longitudinal plane. Left ICA showing a spiculated ﬂ ow signal shortly after the focal stenosis addition- ally indicating a high grade of stenosis (ﬂ ow velocities 95/20 cm/s).

Fig. B15.10 Extracranial duplex, longitudinal plane. Left ICA demonstrating a severe stenotic ﬂ ow signal with marked turbulences and increased ﬂ ow velocities (394/231 cm/s).

M1-MCA-R

Fig. B15.12 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Mildly poststenotic ﬂ ow pattern in the right M1-MCA (ﬂ ow velocity 77/42 cm/s).

304 Case 15 Near-Occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

A1-ACA-R

Fig. B15.13 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Antegrade poststenotic ﬂ ow pattern in the right A1-ACA (ﬂ ow velocity 48/23 cm/s).

OA-R

C6-ICA-R

Fig. B15.14 TCCS (transtemporal approach), right-sided insonation, lower pontine plane. Markedly reduced ﬂ ow signal in the right C6-ICA (ﬂ ow velocity 26/9 cm/s).

P1-PCA-R

Fig. B15.15 TCCS ( tran sorbital appr oach ), righ t-si ded insonat ion: Raised retrograde ﬂ ow in the right OA with an internalized ﬂ ow p a t t e r n ( ﬂ ow velocity 62/26 cm/s).

P2-PCA-R

Fig. B15.17 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normal ﬂ ow velocity in the right distal P2-PCA (ﬂ ow velocity 43/17 cm/s).

Fig. B15.16 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Slightly increased ﬂ ow velocity in the right P1-PCA (ﬂ ow velocity 79/35 cm/s).

PCoA-R

Fig. B15.18 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Mild turbulence and increased ﬂ ow velocity in the right PCoA toward the anterior circulation indicating functional PCoA and collateral ﬂ ow (ﬂ ow velocity 75/30 cm/s).

305Follow-up Neurosonologic Findings (3 Months)

M1-MCA-L

Fig. B15.19 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Poststenotic ﬂ ow pattern in the left M1-MCA (ﬂ ow velocity: 39/21 cm/s).

C6-ICA-L

A1-ACA-L

Fig. B15.20 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Antegrade, slightly poststenotic ﬂ ow pattern in the left A1-ACA with elevated ﬂ ow velocity (98/53 cm/s).

OA-L

(TO)

Fig. B15.21 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , lower pontine plane. Markedly reduced ﬂ ow signal and poststenotic ﬂ ow pattern in the left C6-ICA (ﬂ ow velocity 21/14 cm/s).

OA-L

(TT)

Fig. B15.23 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , upper pontine plane: The left OA is also detected by a transtemporal approach with a retrograde ﬂ ow and internalized ﬂ ow pattern (ﬂ ow velocity 46/14 cm/s). Note the transients (arrows) provoked by tapping of the eye bulb to assure the OA.

Fig. B15.22 TCCS ( tran sorbital a pproach ), lef t-si ded in sona tion: Raised retrograde ﬂ ow in the left OA with an internalized ﬂ ow p a t t e r n ( ﬂ ow velocity 37/12 cm/s).

P1-PCA-L

Fig. B15.24 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Mild increased ﬂ ow velocity in the left P1-PCA (ﬂ ow velocity 91/36 cm/s).

306 Case 15 Near-Occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

P2-PCA-L

Fig. B15.25 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Similar increased ﬂ ow velocities in the left distal P2-PCA indicating leptomeningeal collateral ﬂ ow via the PCA (ﬂ ow velocity 81/32 cm/s).

OTA-L

ATA- L

Fig. B15.26 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Increased ﬂ ow velocities can also be seen in the anterior temporal artery (ATA), a branch of the PCA (ﬂ ow velocity 58/25 cm/s).

Fig. B15.27 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Increased ﬂ ow velocities can also be seen in the occipitotemporal artery (OTA), a further branch of the PCA (ﬂ ow velocity 68/24 cm/s).

Fig. B15.28 DSA, right CCA injection, lateral view. (A) Early ar- terial phase: Note that only a blind ICA sack can be seen, similar to the initial ﬁ ndings in duplex sonography (arrowhead). (B) Late arterial phase: With a delay a marked stenosis (arrowhead) and a residual contrast in a collapsed vessel lumen of the right ICA can be seen (arrows).

ICA-R

307Follow-up Neurosonologic Findings (3 Months)

Fig. B15.29 Schematic of the extra- and intracranial brain-supplying arteries. Right ICA near-occlusion and left 80% ICA stenosis (NASCET). Flow to the right anterior circulation is maintained via the PCoA and OA. Flow for the left anterior circulation is assured via the stenotic ICA, the ipsilateral OA, and the PCA via leptomeningeal collaterals.

ECA-R

Fig. B15.31 Extracranial duplex, longitudinal plane. Right ECA now shows a normalized pulsatile ﬂ ow signal (ﬂ ow velocity 99/12 cm/s, PI = 2.0).

Fig. B15.30 Extracranial duplex, longitudinal plane. Right ICA showing a normalized ﬂ ow signal after stent treatment (ﬂ ow ve- locity 99/33 cm/s). Also, the distal ICA diameter normalized from initially 3.1 mm before stenting to 4.2 mm after the intervention.

M1-MCA-R

Fig. B15.32 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normalized ﬂ ow signal in the right M1-MCA following stenting of the right ICA (ﬂ ow velocity 89/35 cm/s).

A1-ACA-R

Fig. B15.33 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normalized ﬂ ow signal in the right A1-ACA segment with high velocities (116/33 cm/s) indicating activation as

C6-ICA-R

Fig. B15.34 TCCS (transtemporal approach), right-sided insonation, lower pontine plane. Normalized ﬂ ow signal in the right C6- ICA segment (ﬂ ow velocity 92/36 cm/s).

collateral vessel for the contralateral side.

308 Case 15 Near-Occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

OA-R

Fig. B15.35 TCC S (t rans orbital ap proach) , ri ght-sided inson ation: Normalized antegrade ﬂ ow in the right OA (ﬂ ow velocity 68/23 cm/s).

P1-PCA-R

Fig. B15.36 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normalized ﬂ ow signal in the right P1-PCA segment (ﬂ ow velocity 53/23 cm/s) indicating cessation of PCoA activation.

Fig. B15.38 Intracranial 3D TOF-MRA, axial MIP. All visible vessel segments of the ICA, MCA, ACA, PCA, and basilar artery (BA) have a

Fig. B15.37 Schematic of the patient’s extra- and intracranial

similar signal intensity, indicating normalized ﬂ ow. brain-supplying arteries after right-sided ICA stenting. Normalized ﬂ ow from the right ICA toward the anterior circulation. Note that the right A1-ACA is now contributing blood as a collateral toward the left ACA territory.

A1-ACA-R C6-ICA-R

Fig. B15.39 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Lower ﬂ ow velocities in the right A1-ACA seg- ment after left-sided ICA stenting, indicating its previous activation as collateral (ﬂ ow velocity: 66/27 cm/s).

Fig. B15.40 TCCS (transtemporal approach), right-sided insona-

tion, lower pontine plane. Lower ﬂ ow velocities in the right C6-ICA

segment after left-sided ICA stenting, indicating its previous activa-

tion as a collateral (ﬂ ow velocity 51/17 cm/s).

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