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429Final 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.

Clinical Course (2)

Considering the dynamic vascular process, intravenous heparin was started, aiming for a doubling of the partial thromboplastin time (PTT). The new left-sided distal ICA occlusion was ﬁ nally considered to be of atherothrom- botic 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. Biopsy of one branch of the superﬁ cial temporal artery (STeA) revealed no signs of large-vessel arteritis.

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. CT angiography (CTA) ﬁ ndings 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 hyperechoic material occluding the left ICA, ECA, and distal CCA. Color-mode

imaging 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 M1-MCA segment with blood supply from the ipsilateral ICA and via leptomeningeal collaterals from the PCA.

Fig. B30.34 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries.

Final Diagnosis

Marked atherosclerosis with right near-occlusion of the M1-MCA and left M1-MCA stenosis. Secondary left intracranial ICA occlusion and subsequent ipsilateral retrograde CCA thrombosis. Unfavorable collateralization via the cerebral arterial circle (circle of Willis) leading to bilateral internal BZIs.

Fig. B30.1 Cerebral MR T2-weighted image, axial plane. A rosary-like pattern of deep white-matter signal abnormalities in the right corona radiata, consistent with an internal BZI (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 (single arrow). Note the absent signal 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.)

430 Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions

Fig. B30.3 Intracranial 3D TOF-MRA, coronal MIP. Assumed o c c l u s i o n o f t h e r i g h t M 1 - M C A a n d A 1 - A C A s e g m e n t s ( s m a l l 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). Also, the distal left ICA was visible (dotted arrow), contrary to the ce-MRA. (Courtesy of Dr. Grüger, Martin Gropius Krankenhaus, Eberswalde, Germany.)

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 with the left M1-MCA, the diameter appears reduced. (Courtesy of Dr. Grüger, Martin Gropius Krankenhaus, Eberswalde, Germany.)

ICA-L

Fig. B30.5 Extracranial duplex, longitudinal plane (color-mode image). Normal ﬂ ow signal in the left ICA (ﬂ ow velocity 115/56 cm/s). Note the prominent hypoechoic plaque (arrows).

ICA-L

Fig. B30.6 Extracranial duplex, transverse plane (color-mode image). Axial imaging reveals a lumen reduction of the left proximal ICA of ~40–50% caused by a hypoechoic eccentric plaque.

Final Diagnosis

431

ICA-R

Fig. B30.7 Extracranial duplex, longitudinal plane. A distinct reduced ﬂ ow signal was seen in the right ICA (ﬂ ow velocity 24/11 cm/s). Also, a hypoechoic plaque is present (arrows).

M1-MCA-L

ICA-Siphon-L

Fig. B30.8 TCCS (tran stemporal appro ach) , left -sid ed ins onati on, upper pontine plane. Stenotic ﬂ ow pattern in the left carotid siphon (ﬂ ow velocity 228/94 cm/s).

M1-MCA-L distal

Fig. B30.9 TCCS (tran stemporal appro ach) , left -sid ed ins onati on, midbrain plane. Stenotic ﬂ ow pattern in the left proximal M1-MCA (ﬂ ow velocity 221/131 cm/s).

A1-ACA-L

Fig. B30.11 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. High velocities and a turbulent and poststenotic ﬂ ow pattern in the left A1-ACA probably supplying both A2-ACAs (ﬂ ow velocity 132/69 cm/s).

Fig. B30.10 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Mild poststenotic ﬂ ow pattern in the distal left M1-MCA (ﬂ ow velocity 65/25 cm/s).

MCA-R

PCA-R

A1-L

Fig. B30.12 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Color-ﬂ ow image of the circle of Willis with strong left A1- and both A2-ACAs and missing right A1-ACA (arrow). Note the good red-colored image of the right M1-MCA and the accompanying blue-coded deep middle cerebral vein (arrowhead). Note also the prominent signal of the right proximal PCA.

432 Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions

M1-MCA-R

Fig. B30.13 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Stenotic ﬂ ow pattern with increased and turbulent ﬂ ow in the right proximal M1-MCA (ﬂ ow velocity 161/74 cm/s).

P1-PCA-R

M2/M3-MCA-R

Fig. B30.14 TCCS (transtemporal approach), right-sided insonation, thalamic plane. Severe poststenotic ﬂ ow pattern in one right M2/M3-MCA branch (ﬂ ow velocity 58/33 cm/s).

Fig. B30.15 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Prominent ﬂ ow in the right P1- and P2-PCA, indicating leptomeningeal collateralization. Here the P1-PCA is shown (ﬂ ow velocity 159/88 cm/s).

Fig. B30.16 DSA, left CCA injection, posteroanterior view. Proximal ICA stenosis of ~50% (arrowhead).

Final Diagnosis

433

Fig. B30.17 DSA, right ICA injection, posteroanterior view, late

arterial 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 ﬁ ne network of lenticulostriate vessels (arrows).

Fig. B30.19 DSA, right VA injection, posteroanterior view. Collateral leptomeningeal ﬂ ow to the right MCA territory via the right PCA (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. B30.20 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). Note the left-sided distal siphon stenosis (small arrowhead) and the proximal M1-MCA stenosis (large arrowhead).

434 Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions

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 ﬁ lling 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. No retrograde MCA collateral ﬁ lling via the ACA and PCA was seen.

Fig. B30.22 Schematic of the patient’s extra- and intracranial brain-supplying arteries (initial ﬁ ndings). Near-occlusion of the right M1-MCA (circle) and missing A1-ACA. Leptomeningeal collateral blood ﬂ ow to the 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 stenoses (circles).

Fig. B30.23 Cerebral MR FL AIR image, axial plane. More conﬂ uent- like pattern in the left corona radiata, consistent with a new contralateral internal BZI.

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 ﬁ ndings on the right side.

ICA-L

Final Diagnosis

435

Fig. B30.25 Intracranial 3D TOF-MRA, now revealing an absent left

ICA signal. Reduced signal in both proximal MCAs (arrows) as well as in the distal ACAs (arrow). The right intracranial ICA is still visible (arrowheads). The vertebrobasilar arteries and both PCAs revealed a prominent signal indicating elevated ﬂ ow.

M1-MCA-L

Fig. B30.27 TCC S (tr ans tempo ral a ppro ach) , l eft -sid ed in sona tion , midbrain plane. Stenotic ﬂ ow pattern of the left M1-MCA, but ﬂ ow velocities had decreased in comparison to the preceding investigation (ﬂ ow velocity 81/46 cm/s). Note also a mild poststenotic ﬂ ow pattern.

Fig. B30.26 Extracranial duplex, longitudinal plane. High-resistance ﬂ ow signal in the left ICA with a low and short systolic ﬂ ow and completely absent diastolic ﬂ ow component consistent with distal occlusion.

A1-ACA-L

Fig. B30.28 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. The left A1-ACA showed an antegrade, but marked poststenotic ﬂ ow pattern with obviously reduced ﬂ ow velocity compared with the ﬁ rst examination (ﬂ ow velocity 53/33 cm/s).

P1-PCA-L

Fig. B30.29 TCCS (tran stempor al a pproach ), lef t-sid ed insonation, midbrain plane. Raised ﬂ ow velocities in the left P1-PCA (ﬂ ow velocity 190/99 cm/s).

PCoA-L

Fig. B30.30 TCC S (tr anste mpor al ap proa ch), lef t-side d ins onat ion, upper pontine plane. Turbulences in the left PCoA, indicating collateralization of the left MCA and both ACA territories via the left PCoA.

436 Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions

Fig. B30.31 TCCS ( tran sforami nal approa ch), upper ax ial pl ane. Marked nonturbulent ﬂ ow in the BA (ﬂ ow velocity 208/108 cm/s).

Fig. B30.32 Intracranial CTA, axial MIP. Left M1-MCA stenosis ( a r r o w h e a d ) a n d r i g h t M 1 - M C A n e a r - o c c l u s i o n ( a r r o w ) . N o t e t h a t both A2-ACAs are supplied by a prominent left A1-ACA. Note also that the left PCoA is not visualized. In contrast, the deep middle cerebral vein can be seen (dotted arrow).

CCA-L

Fig. B30.33 Extracranial duplex, longitudinal plane. Color-mode image revealed no ﬂ ow signal. Doppler spectrum analysis showed a stump signal in the proximal CCA. Note the echogenic material within the distal CCA (arrows).

Fig. B30.34 Schematic of the patient’s extra- and intracranial brain-supplying arteries (ﬁ ndings at follow-up). Persisting near- occlusion of the right M1-MCA (circle). Persisting leptomeningeal collateral blood ﬂ ow to the right MCA territory from the right PCA (green arrow). Left extracranial ICA, CCA, and ECA occlusion ( c i r c l e ) . P e r s i s t i n g l e f t i n t r a c r a n i a l M C A s t e n o s i s . C o l l a t e r a l b l o o d ﬂ ow for the left MCA and both ACA territories is from the posterior circulation via the left PCoA.

437Discussion

Discussion

Clinical Aspects

This is an instructive case of a 41-year-old woman, which gives insights into the topic of BZI. It also illustrates the strengths and weaknesses of the currently available angiologic methods to assess intracranial high-grade stenosis or near-occlusion in cases of complex multilocular steno-occlusive disorders.

Our patient initially presented with repeated sensory TIAs which, because of their repeated and monomorphic pattern, were suggestive of hemodynamic events. Correspondingly, MRI detected an internal BZI on the right side, presumably due to a near-occlusion of the right MCA. Thirty days later she developed a large second internal BZI on the contralateral side, which led to severe akinetic mutism. She was unable to communicate although her sensorimotor functions remained unchanged. Over time, spontaneous speech function reappeared to a minimal level. Akinetic mutism following stroke can be caused by lesions in diﬀ erent regions of the brain but most frequently it occurs in cases with damage of the anteromedial frontal lobes (Nagaratnam et al 2004). Bilateral anterior cerebral infarction can lead to complete and persisting akinetic mutism (Freemon 1971, Minagar and David 1999). Akinetic mutism as a result of bilateral internal BZIs has not yet been reported.

BZIs, also called “watershed infarctions,” are caused by a low ﬂ ow state in large brain-supplying arteries. Clinical and autopsy studies suggest that up to 10% of brain infarctions are of hemodynamic origin (Bladin and Chambers 1994, Jörgensen and Torvik 1969). BZI may occur in the anterior or in the posterior circulation along the boundaries between the vascular territories of the major intracranial vessels. However, the exact nature and signiﬁ cance of border zone lesions are still being de- bated (Momjian-Mayor and Baron 2005). Infratentorial BZI of the cerebellum is less well understood and is not be discussed further here (Amarenco et al 1993, De Cocker et al 2013). Supratentorial BZI occurs in high-grade stenosis or occlusion of the ICA or MCA or occasionally in cases with a profound temporary hypotension. In general, two types of infarcts, external and internal BZIs, can be distinguished. External BZIs present as wedgeshaped cortical/subcortical lesions localized between the ACA and MCA territory (anterior external BZIs) and the MCA and PCA, or MCA, PCA, and ACA territory (posterior external BZIs). They are also called cortical BZIs. In occlusive ICA disorders, mainly anterior external BZIs are observed. A posterior external BZI may be present in fetal-type PCA or in the case of additional steno-occlusive disease in the vertebrobasilar circulation. Interestingly, there are no clear-cut data on the correlation between the distribution of cortical BZIs and vessel status. The internal border zone involves a subcortical area in the corona radiata between the superﬁ cial and deep perfo- rators of the MCA or between the superﬁ cial perforators of the MCA and ACA which represents the most distal part of ICA perfusion.

Internal BZIs may appear rosary-like, i.e., forming a line of small white-matter lesions, or in the form of a prominent cigar-shaped conﬂ uent pattern (Bladin and Chambers 1993). The two infarct patterns may occur separately or together (for further detail see Chapter 4, “Border Zone Infarction” under “Arterial Ischemia”).

Diagnostically, clear diﬀ erentiation between an ex- ternal BZI and a territorial infarction near the territorial border is often diﬃ cult. This is particularly true as these borders show a great variability depending on the variants of the circle of Willis even under physiologic circumstances (van der Zwan et al 1992, van Laar et al 2006a). In chronic occlusive disease (e.g., chronic ICA occlusion) this border might be shifted further, resulting in a smaller MCA territory. In this constellation, an external BZI may appear morphologically as a cortical territorial infarction. But even in infarctions that are clearly localized within the border zone, it may still be debatable whether the underlying cause is hemodynamic or embolic or a combination of both (Caplan and Hennerici 1998). A hypothesis for combined pathogenesis is that emboli are more likely to develop and are at the same time less likely to subsequently disintegrate in low ﬂ ow regions, such as the border zones, afterwards leading to embolic infarcts within the borders. A diﬀ usion-weighted MR study sup- ports the above hypothesis of embolic mechanisms, at least for external BZIs. The authors compared 45 patients with internal BZIs and 75 patients with external BZIs. The latter patients had smaller cortical infarct patterns and fewer steno-occlusive altered vessels. In people with internal BZIs, a rosary-like infarct pattern was found and more underlying ICA or MCA steno-occlusive pathology was present. Occlusion or marked stenosis (≥50%) was found in 91.1% of patients with internal BZIs, but in only

73.3% of patients with external BZIs. The authors concluded that embolism may therefore have a greater role in external BZIs and that acute hypotensive events may be of more relevance in internal BZIs (Yong et al 2006). Several studies have been initiated to further analyze the underlying pathomechanism and to question or prove the embolic hypothesis, combining the assessment of large-vessel status, ultrasound embolus detection, and diﬀ usion-weighted MRI. In MCA stenosis, microembolic signals were more frequently observed in patients with multiple lesions on diﬀ usion-weighted MRI, especially along the border zones, which were considered to be caused by impaired disruption and clearance of emboli (Wong et al 2002).

Angiologic Aspects

Our patient had severe atherosclerotic disease consisting of multiple high-grade stenoses and occlusions aﬀ ecting the intra- and extracranial brain-supplying arteries, but obviously sparing the posterior circulation.

The assessment of extracranial high-grade stenosis or near-occlusion, for example of the ICA, may pose questions, and this is discussed in Case 15. It is therefore not surprising that imaging and assessment of intracranial

438 Case 30 Multilocular Extra- and Intracranial Stenoses and Occlusions

high-grade stenosis and near-occlusion seems even more diﬃ cult because of the smaller vessel diameters (for fur- ther details see Case 25). The problem can be illustrated by comparing the diﬀ erent evaluations of the constant right M1-MCA vascular pathology in our patient. The TOF-MRA initially performed suggested a right proximal M1-MCA occlusion and an A1-ACA occlusion. Careful assessment of the images revealed signals of the most proximal part of the M1-MCA and A1-ACA segments, as well as an opercular branch. In the long segment between both branches no signal was seen. Such a long “gap sign” in TOF-MRA is usually considered to represent occlusion, whereas a short gap frequently coincides with a highgrade stenosis. However, this is a rough measure only and results in high interobserver variability. Accordingly, an MRI study that compared TOF-MRA and ce-MRA revealed great discrepancies in ﬁ ndings of assumed main-stem and branch occlusion (Yang et al 2005). Apart from ceMRA, analysis of source images may be helpful in proving vessel patency. In our experience it is also always valuable to analyze standard T2-weighted images. In our patient, a long-segmented signal void was clearly visible within the main stem of the right MCA, indicating a patent vessel and at least a residual ﬂ ow (see Fig. B30.4).

DSA was the second technique to be used to further analyze the presumed proximal M1-MCA and A1-ACA occlusion. The early arterial images seemed to conﬁ rm the diagnosis but on evaluation of the late arterial phase, insular MCA branches, probably a very temporal branch, and lenticulostriate arteries became visible, rather suggestive of an MCA near-occlusion (see Fig. B30.17). Ret- rograde MCA ﬁ lling through leptomeningeal collaterals from the ACA and the PCA was not seen. Therefore, M2 and M3 branches that became visible after right CCA injection had to be supplied by the ICA itself. Currently, DSA is the reference method for imaging of intracranial vessels. However, false-negative ﬁ ndings have also been reported with this technique: for example, in low ﬂ ow vessel segments in patients with moyamoya disease when compared with ultrasound (Muttaqin et al 1993, Ruan et al 2006) (see also Case 9), and also in distal near-occlusion of the BA in comparison to CTA (Bash et al 2005). As in our patient presenting low ﬂ ow due to atherosclerotic artery disease, false-negative results might occur if only early arterial phase images are analyzed. Therefore, evaluation of the late arterial phases is mandatory, so that low ﬂ ow states in suspected occlu- sion are not overlooked.

The third technique to be used was CTA. Similar to MRA and early arterial DSA images, CTA maximal intensity projection (MIP) images revealed a signal gap within the right M1-MCA segment visible in the axial and the coronal planes. Based on CTA alone, a unilateral right MCA occlusion would probably have been the (wrong) ﬁ nal diagnosis. In addition, CTA did not reveal the left-sided PCoA which is the crucial vessel for the left MCA and both ACA territories (see Fig. B30.22). Nowadays time-resolved analysis with thin-slice 4D CTA data makes it possible to show the presence of antegrade contrast opaciﬁ cation distal to the primary assumed occluded vessel segment. In the acute stroke setting a

residual ﬂ ow in a near-occluded vessel may obviously predict early vessel recanalization compared with a deﬁ - nite occlusion (Frölich et al 2012).

In this special case ultrasound was superior to the angiographic techniques as it demonstrated a longsegmental antegrade M1-MCA segment on color-mode imaging (see Fig. B30.12). Flow velocity in the proximal right M1-MCA was increased to values found in moderate stenoses (ﬂ ow velocity 161/74 cm/s). The marked post- stenotic ﬂ ow pattern of the subsequent vessel segments changed our interpretation to the presence of a hemodynamically relevant high-grade stenosis.

Next, discrepant angiologic results were seen regarding a complete left CCA, ECA, and ICA occlusion seen in extracranial ce-MRA. While the ECA occlusion was real, the CCA and proximal ICA were open on duplex ultrasound examination. However, they had a severe high-resistance ﬂ ow pattern with low systolic ﬂ ow and missing diastolic ﬂ ow indicative of a distal ICA occlusion. The re- duced ﬂ ow wrongly led to a picture of complete left-sided carotid arteries occlusion.

Besides the analysis of stenoses and occlusions, hemodynamic eﬀ ect and the subsequently induced collateral pathways pose another challenge for imaging. Collateral function and stroke are closely related. Functional ultrasound analysis using a CCA compression test revealed that a nonfunctional ACoA/PCoA was present in 33%/57% of cases in a stroke patient population but only in 6%/43% of healthy controls (Hoksbergen et al 2003a), implying that individuals with hypoplastic or aplastic (i.e., nonfunctional) communicating arteries may be more likely to have an ischemic stroke. Also, in stroke patients, the quality of collateral function has been shown to have considerable inﬂ uence on the clinical outcome. A DSA study in acute anterior circulation occlusion showed that favorable collateralization had a higher odds ratio than successful recanalization (5.9 versus 1.9) in terms of a good clinical outcome (Kucinski et al 2003).

Direct imaging of the communicating arteries that contribute as collaterals in occlusive vessel disorders might be diﬃ cult when using TOF-MRA or CTA. In our case, for example, neither of the techniques was able to depict the signal of the important left PCoA. This can be explained by the ﬂ ow sensitivity of TOF-MRA, impairing the detection of raised turbulent ﬂ ow. With CTA analysis, the imaging of small vessel segments might be a question of choosing the right postprocessing technique. Consideration of source images might also be helpful. Transcranial color-coded duplex sonography (TCCS) is superior if a suﬃ cient acoustic bone window is present. In our

ow t

case collateral blood ﬂ

o the left MCA and ACA was provided by the left PCoA, which yielded a strong, highly turbulent ﬂ ow on TCCS evaluation. If no direct insonation is possible, indirect sonographic signs may be used to prove the collateral ﬂ ow pattern. Increased ﬂ ow veloci- ties within the P1-PCA segment and almost normal ﬂ ow velocities in the P2- and P3-PCA segments in a patient with extra cranial ICA occlusion point to a direct PCoA collateral function. Raised ﬂ ow velocities in the distal PCA segments starting at the P1-PCA segment indicate a leptomeningeal collateralization.

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