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329Initial Neurosonologic Findings (Day 3)

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

Fig. B18.5 DSA, right selective VA injection, posteroanterior view. Undisturbed vertebrobasilar ﬂ ow. Note the prominent ﬁ lling of the right MCA and ACA vessels (arrows) indicating leptomeningeal collateral ﬂ ow via the PCA.

Fig. B18.7 Schematic of the patient’s extra- and intracranial brain-supplying arteries on day 2 before the ﬁ rst DSA with assumed right M1-MCA occlusion.

Fig. B18.6 DSA, right selective distal ICA injection, posteroanterior view. (A) Proximal right MCA occlusion but open ipsilateral ACA at this time point. (B) Final result after treatment with stent retriever and suction systems revealing a reopened MCA (arrows).

Fig. B18.8 Schematic of the patient’s extra- and intracranial brain-supplying arteries directly after mechanical thrombectomy of the right M1-MCA occlusion.

widely in diﬀ erent segments of the V2-VAs (right V2-VA between 100/75 cm/s and 294/148 cm/s, left V2-VA between 44/38 cm/s and 408/216 cm/s) primarily suggestive of multiple stenoses (Fig. B18.13). Blood volume ﬂ ow measurements of the V2-VA revealed high values of 258 mL/min in the right and 152 mL/min in the left V2-VA (Fig. B18.14). Together with a high diastolic ﬂ ow compo- nent the ﬁ ndings were interpreted as an additional com- pensatory vertebrobasilar hyperperfusion to collateralize the right-sided ICA occlusion and the suspected severe steno-occlusive lesion in the distal left ICA.

both M1-MCA indicating collateral ﬂ ow via the OA (see Fig. B18.24). The main collateral pathway was via both posterior communicating arteries (PCoAs) indicated by elevated ﬂ ow velocities in both P1-PCA segments (right P1-PCA 103/60 cm/s; left P1-PCA 133/82 cm/s) and n o r m a l v a l u e s i n b o t h P 2 - P C A ( r i g h t P 2 - P C A 3 1 / 1 7 c m / s ; left P2-PCA 46/30 cm/s) as well as a functional stenosis in both PCoAs with a ﬂ ow direction toward the a n t e r i o r c i r c u l a t i o n ( r i g h t P C o A 1 1 2 / 6 9 c m / s ; l e f t P C o A 143/106 cm/s) (Fig. B18.16, Fig. B18.17, Fig. B18.18). The C6-ICA was undetectable on both sides. Right and left OA showed an internalized and retrograde ﬂ ow signal with

Transcranial Duplex Sonography

The right M1-MCA was open. Doppler spectra of both M1-MCA and A1-ACA segments showed a moderate poststenotic ﬂ ow pattern (Fig. B18.15). Digital tapping of the ipsilateral ocular bulb led to typical transients on

markedly elevated ﬂ ow velocities (right OA 52/26 cm/s; left OA 89/39 cm/s) (Fig. B18.19 and Fig. B18.20). Elevated ﬂ ow velocities with low pulsatility were seen also in both V4-VA segments (right V4-VA 120/71 cm/s; left V4-VA 63/47cm/s) and in the basilar artery (BA) (89/58 cm/s) suggestive of hyperperfusion (not shown).

330 Case 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle

Cerebral Artery Occlusion

CCA-R

Fig. B18.9 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right CCA with reduced ﬂ ow velocity and in- creased pulsatility (ﬂ ow velocity 69/7 cm/s, PI = 3.7).

ECA-R

ICA-R

Fig. B18.10 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right ICA revealing a low velocity and increased pulsatility (ﬂ ow velocity 18/0 cm/s) compatible with an infraoph- thalmic ICA occlusion. Note the reduced diameter of the ICA without direct signs of dissection at this level (arrows).

ICA-L

Fig. B18.11 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right ECA revealing an “internalized” ﬂ ow signal with a low pulsatility (ﬂ ow velocity 56/12 cm/s, PI = 2.1).

Conclusion

Traumatic four-vessel dissection with steno-occlusive infraophthalmic lesions of both ICAs and with multisegmental stenoses of both VAs. Additional bilateral VA hyperperfusion due to collateral function via the PCoAs toward the anterior circulation as well as additional collateral ﬂ ow via both OAs.

Clinical Course (2)

The patient’s condition remained stable with further slight improvement of the hemiparesis and aphasia. Because of the suspected steno-occlusive lesion of the left ICA not seen before, a second DSA was performed.

Fig. B18.12 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the left ICA demonstrating direct signs of a dissecting lesion with a distal vessel widening (dotted lines) due to an intramural hematoma (arrows), subsequently causing a marked local stenosis. Despite this, only a low ﬂ ow velocity and a high pulsatility was seen and considered as indirect signs of an additional ﬂ ow obstruction with further distal location (ﬂ ow velocity 55/9 cm/s, PI = 2.1)

Second Conventional Angiography (Day 4)

The second DSA conﬁ rmed a right-sided submandibular rat-tail-like ICA occlusion with collateral supply of the still open MCA and ACA territory via the PCoA and retrograde right OA. The left ICA now revealed a long-segmented extracranial stenosis beneath the known small dissecting aneurysm. However, the major ﬁ nding was a new circum- scribed high-grade left ICA stenosis in the petrosal part at the junction between the vertical and horizontal segment. There was also a progressed lumen reduction in the left VA, which was important as the main collateral ﬂ ow into both anterior circulations was ensured by the vertebrobasilar circulation (Fig. B18.21, Fig. B18.22, Fig. B18.23).

331Follow-up Neurosonologic Findings (Day 21)

V2-VA-L

Fig. B18.13 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the left V2-VA with vessel widening (dotted lines) due to an intramural hematoma (arrows) with a maximum of stenosis at the entrance of transverse process C5. Flow velocity was very high (408/216 cm/s) primarily indicating a severe stenosis.

M1-MCA-R

V2-VA-L

Fig. B18.14 Extracranial duplex, longitudinal plane. Doppler spectrum analysis and volume ﬂ ow measurement of the left V2-VA. A poststen- otic ﬂ ow pattern was seen between C3 and C4 assuring a hemody- namic relevant V2-VA stenosis. However, volume ﬂ ow analysis showed a high ﬂ ow despite a moderate vessel lumen of 3.9 mm, considered to reﬂ ect additional collateral ﬂ ow toward the anterior circulation.

P1-PCA-R

Fig. B18.15 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Poststenotic ﬂ ow pattern and reduced veloci- ty in the right M1-MCA (ﬂ ow velocity 58/35 cm/s).

Fig. B18.24 shows a schematic of the patient’s extra- and

intracranial brain-supplying arteries after the second DSA.

Fig. B18.16 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Increased ﬂ ow velocity in the right P1-PCA, indicating collateral ﬂ ow (ﬂ ow velocity 103/60 cm/s).

left ICA, indicating resolution of the distal ICA obstruction and/or hyperperfusion for collateral ﬂ ow toward the o c c l u d e d r i g h t I C A ( ﬂ ow velocity 133/84 cm/s). Flow

Clinical Course (3)

The patient’s neurologic symptoms continued to improve.

velocities in both VA were lower than in the previous ultrasound assessment (right VA 126/61 cm/s; left VA 173/91 cm/s) (Fig. B18.25 and Fig. B18.26).

PTT-guided heparin treatment was changed to oral anticoagulation with phenprocoumon 2 weeks later. After 4 weeks the patient was transferred to a rehabilitation center with a mild residual left-sided hemiparesis (NIHSS 5).

Transcranial Duplex Sonography

The left OA returned to be antegradely perfused. No other relevant variations compared with the previous

Follow-up Neurosonologic Findings

examination were seen.

(Day 21)

Extracranial Duplex Sonography

The right ICA remained occluded. The size of the left intramural ICA hematoma had decreased. Doppler spectrum analysis revealed an increase of ﬂ ow velocities in the

Conclusion

Persistent right ICA occlusion. Partial regression of left ICA and left VA lumen narrowing indicating the restitution process of the aﬀ ected vessels.

332 Case 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle

Cerebral Artery Occlusion

P2-PCA-R

Fig. B18.17 TCCS (transtemporal approach), right-sided insonation, thalamic plane (inverse color mode and Doppler mode). Normal ﬂ ow in the distal right P2-PCA (ﬂ ow velocity 31/17 cm/s). Therefore, collateral ﬂ ow was assumed to run via the PCoA and not via leptomeningeal collaterals.

OA-R

PCoA-R

Fig. B18.18 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Turbulent and increased ﬂ ow velocity with ﬂ ow toward the probe in projection of the right PCoA, corresponding to a functional stenosis (ﬂ ow velocity 112/69 cm/s) caused by collateral ﬂ ow toward the anterior circulation.

OA-L

Fig. B18.19 TCCS ( tran sorbital appr oach ), righ t-si ded insonat ion. Raised retrograde ﬂ ow in the right OA with an internalized ﬂ ow pat- tern (ﬂ ow velocity 52/26 cm/s).

Follow-up MRI and MR Angiography (8 Months)

MRI of the brain conﬁ rmed the known partial territo- rial MCA infarction in the right hemisphere. No further ischemic or hemorrhagic lesions had developed. Intracranial time-of-ﬂ ight MR angiography (TOF-MRA) revealed the persistent distal right ICA occlusion. Normal ﬂ ow signals were found in the left intracranial ICA and in all basal cerebral arteries on both sides except for a severe vessel narrowing of the right A1-ACA (Fig. B18.27)

Fig. B18.20 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 pat- tern (ﬂ ow velocity 88/39 cm/s). Note the bidirectional ﬂ ow signal caused by an elongated OA course. This ﬁ nding may cause insecu- rity regarding the “true” ﬂ ow direction. However, the clearly inter- nalized ﬂ ow pattern together with the extracranial duplex ﬁ ndings assure the presence of a retrograde ﬂ ow direction toward the brain.

Follow-up Neurosonologic Findings (After 1 Year)

Extracranial Duplex Sonography

The right ICA remained occluded revealing a long-segmented blind sack and a “stump signal” (see Fig. B18.20). Complete normalization was observed in the detectable left ICA and both VAs (not shown).

Transcranial Duplex Sonography

Flow in the right M1-MCA was normal, receiving blood via the right PCoA, indicated by an increased right P1-PCA and increased right PCoA ﬂ ow velocity. Interestingly, the

333Follow-up Neurosonologic Findings (After 1 Year)

Fig. B18.21 (A) DSA, right selective ICA injection, posteroanterior view, showing the typical rat-tail-like occlusion of the ICA at the entrance to the skull base (arrows). (B) DSA, left selective ICA injection, posteroanterior view. Unchanged small aneurysm (arrowhead) with a more prominent ICA tailoring (arrows). The major ﬁ nding, however, was a severe stenosis at the border between the vertical and horizontal course of the petrosal ICA (arrow).

A B

B CA

Fig. B18.22 (A) DSA, left selective ICA injection, posteroanterior view, showing the hemodynamic signiﬁ cance of the proximal C6-ICA stenosis (arrow). An embolic cause seemed unlikely because of its location. As the DSA 2 days prior had demonstrated a mild contrast ﬁ lling, an increasing wall hematoma during anticoagulation was assumed. The weak MCA and ACA contrast ﬁ lling indicates its hemodynamic signiﬁ cance. (B,C) DSA, left selective ICA injection, lateral (B) and oblique (C) view illustrating the high-grade stenosis (arrows).

Fig. B18.23 (A) DSA, superimposed right and left selective VA injection, posteroanterior view. Note a progression of both stenoses now leading to a moderate right and a severe left V2-VA lumen reduction (arrows). (B) DSA, selective left VA injection, posteroanterior view. Note that the posterior circulation provides blood supply toward the anterior circulation with contrast ﬁ lling of both MCA and ACA territories.

right A1-ACA demonstrated a biphasic ﬂ ow signal with a predominantly antegrade ﬂ ow component. An increased ﬂ ow velocity was seen in the left A1-ACA. Together with a functional stenosis in the anterior communicating a r t e r y ( A C o A ) t h e ﬁ ndings were interpreted as a divided collateral ﬂ ow: the right MCA receiving its blood supply from the right P1-PCA (via the PCoA) and the right ACA its blood supply from the left A1-ACA (via the ACoA). The left P1-PCA and PCoA now presented normal ﬂ ow signals. OA ﬂ ow signals on both sides were now antegrade. The right

Fig. B18.24 Schematic of the patient’s extra- and intracranial brain-supplying arteries on day 3 with secondary severe intracranial ICA stenosis on the left side.

Conclusion

Complete recanalization of the left ICA and of both VAs 12 months after traumatic dissection. Persistent right ICA occlusion with a patent but divided intracranial collateral ﬂ ow via the left A1-ACA and ACoA to the contralateral A2-ACA and via the right PCoA to the right M1-MCA.

Fig. B18.39 shows a schematic of the patient’s extraand intracranial brain-supplying arteries after the last duplex ultrasound examination.

OA, however, revealed a mild poststenotic ﬂ ow pattern (Figs. B18.28–B18.37).

334 Case 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle

Cerebral Artery Occlusion

ICA-L V2-VA-L

Fig. B18.25 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the left ICA demonstrating stenosis with a partial restitution of vessel lumen after 3 weeks of disease (arrows). High velocities and an almost normal pulsatility indicated absence of any hemodynamically relevant distal ICA obstruction (ﬂ ow velocity 148/82 cm/s, PI = 0.63).

Fig. B18.27 3D TOF-MRA, axial plane. Absent ﬂ ow signal in the dis- tal right ICA, indicating persistent vessel occlusion. Severe vessel narrowing of the right A1-ACA. Normal ﬂ ow signals in the left ICA, ACA, and BA as well as in both MCAs and PCAs.

Fig. B18.26 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the left V2-VA which now also shows partial vessel restitution (ﬂ ow velocity 173/91 cm/s).

ICA-R

Fig. B18.28 Extracranial duplex, longitudinal plane. B-mode revealing tapering of the right ICA without signs of atherosclerotic changes or typical dissecting features. A stump signal was seen in the Doppler mode, indicating occlusion (not shown).

Clinical Course (4)

The mild left-sided hemiparesis recovered completely within 12 months and the patient had developed no further neurologic symptoms. She continued to take aspirin after 3 months of oral anticoagulation.

Discussion

Clinical Aspects

Here we discuss a patient with traumatic dissection of all cervical brain-supplying arteries caused by a severe car accident. The multiple CADs led to permanent rightsided ICA occlusion and reversible high-grade left ICA and

Final Diagnosis

Tra umati c cer vi cal ar ter y d issec tion of a ll fo ur br ain -supplying arteries with persistent right ICA occlusion and restitution in the other aﬀ ected arteries.

bilateral VA stenoses. The term “traumatic CAD” indicates a CAD caused by a severe blunt and nonpenetrating trauma of the cervical arteries. In contrast, CAD in association with mild mechanical stress such as sport activities, sudden head movements, or coughing is deﬁ ned as “spontaneous

335Discussion

M1-MCA-L

Fig. B18.29 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Normalized ﬂ ow signal in the left M1-MCA (ﬂ ow velocity 100/56 cm/s).

A1-ACA-R

A1-ACA-L

Fig. B18.30 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Elevated ﬂ ow velocity in the left A1-ACA (ﬂ ow velocity 135/71 cm/s) indicating cross-ﬂ ow.

ACoA

Fig. B18.31 TCCS ( tran stempor al approac h), left-sided insonation, midbrain plane. Bidirectional ﬂ ow signal in the right A1-ACA

with an almost antegrade ﬂ ow compatible with a watershed phe- nomenon between the left and right anterior circulation.

CAD,” although the separation into spontaneous or traumatic CAD may arbitrary in some cases (Nedeltchev and Baumgartner 2005). For further reading on spontaneous dissection of the ICA, see mainly Case 11 and Case 20; for spontaneous dissection of the VA, see Case 19.

The reported incidence of traumatic CAD after blunt head and neck trauma is ~0.01–1% (Majidi et al 2014, Nedeltchev and Baumgartner 2005). As in spontaneous CAD, the ICAs are more often aﬀ ected than the VAs (Nedeltchev and Baumgartner 2005). Abrupt rotation or hyperextension of the neck leads to a mechanical stretching of the arteries (Hufnagel et al 1999, Schievink 2001) with potential rupture of the vasa vasorum and bleeding into the vessel layers. Another mechanism of traumatic and spontaneous CAD is an intimal tear with subsequent entering of blood between the layers of the wall of the artery forming an i n t r a m u r a l h e m a t o m a ( C . K . L e e e t a l 2 0 0 9 ) .

Neurologic manifestations of traumatic and spontaneous CAD are similar and vary widely. Beside asymptomatic courses and symptoms directly related to

Fig. B18.32 TCCS (transtemporal approach), right-sided insonation, midbrain plane. ACoA revealing only a mild turbulent ﬂ ow compatible with a good vessel diameter.

M1-MCA-R

Fig. B18.33 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Despite remaining right-sided ICA vessel occlusion normal ﬂ ow signal in the right M1-MCA (ﬂ ow velocity 77/34 cm/s) indicating patent collateral pathways.

336 Case 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle

Cerebral Artery Occlusion

P1-PCA-R

Fig. B18.34 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Remaining increased ﬂ ow velocity in the right P1-PCA, indicating collateral ﬂ ow (ﬂ ow velocity 114/62 cm/s).

PCoA-R

Fig. B18.36 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Turbulent and only mildly increased ﬂ ow ve- locity in the right PCoA indicating collateral ﬂ ow to the right-sided anterior circulation.

the injured vessel (e.g., as local or facial pain, headache, and Horner’s syndrome) any deﬁ cit caused by cerebral ischemia may occur. The absent of any neurologic deﬁ cit is even described after traumatic dissection of all four brain-supplying arteries (Pröscholdt et al 2014). A time interval between the trauma and neurologic symptoms of several hours or even days, as in our patient, is typical for traumatic CAD and may lead to delayed identiﬁ cation with potentially fatal consequences (Galtés et al 2012).

Cerebral infarction in CAD is mainly caused by a r t e r y - t o - a r t e r y e m b o l i s m . E m b o l i c e v e n t s o c c u r i n ~ 8 0 % within the ﬁ rst week after the ﬁ rst symptoms (local signs and/or transient ischemic attacks) and rarely later than 1 month (Biousse et al 1995). Border zone infarctions (BZIs) due to hemodynamic failure occur in only ~5% of patients with CAD (Benninger et al 2004). However, the incidence of BZIs increases up to 16% in patients with high-grade stenosis or occlusion of the ICA (Steinke et al

1996). As BZIs are related to an insuﬃ cient intracranial collateral function, patients with multiple dissections and impaired collateral function of the circle of Willis (hy-

P2-PCA-R

Fig. B18.35 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Normal ﬂ ow in the distal left P2-PCA (ﬂ ow velocity 49/28 cm/s).

poplasia or aplasia of the ACoA, A1-ACA, PCoA, or P1-PCA) have a higher risk of developing hemodynamically related brain infarcts (Hoksbergen et al 2003a). Interestingly, our patient did not develop BZIs and showed an excellent neurologic outcome after several months, although all brain-supplying arteries of the neck were aﬀ ected. This is mainly explained by the large collateral ﬂ ow via the pat- ent P1-PCAs and PCoAs in combination with the bilateral retrograde OA ﬂ ow, which allowed a suﬃ cient perfusion of the anterior circulation. This observation is well in line with recent studies describing no diﬀ erences of function- al outcome after 3 months between patients with single and multiple CAD (Béjot et al 2014).

Recanalization after dissection starts in the majority of patients within the ﬁ rst days and weeks and ﬁ nalizes within months (Steinke et al 1994). A partial or complete restitution was observed in 71% of patients in a study with 24 mainly traumatic VA dissections, which indicates that recanalization rates in spontaneous and traumatic dissections are similar (Bartels and Flügel 1996). Most patients with a traumatic CAD have a favorable prognosis similar to nontraumatic CAD. If diﬀ erences were pres- ent these were related to associated traumatic brain and body lesions (Engelter et al 2013, Mokri 1990, Nedeltchev and Baumgartner 2005). Multiple CADs do not seem to be a predictor for an unfavorable prognosis. A recently published study with 983 CAD patients found a similar functional 3-month outcome in patients with single and multiple CADs (Béjot et al 2014).

In the special case of traumatic CAD the potential beneﬁ t of antithrombotic treatment has to be balanced individually with the risk of bleeding from traumatized tissues (Nedeltchev and Baumgartner 2005). Consequently, early anticoagulation is usually not recommended. Intravenous thrombolysis is also not recommended in traumatic CAD due to the increased risk of intracranial and systemic hemorrhage (Nedeltchev and Baumgartner

2005). In our patient, thrombolysis was not performed because of the preceding serious trauma with surgical intervention, the unknown onset of the MCA stroke, and the delineation of an MCA infarction on cranial CT. A mechanical thrombectomy of the right proximal MCA

337Discussion

OA-R

Fig. B18.37 TCCS ( tran sorbital appr oach ), righ t-si ded insonat ion. Antegrade ﬂ ow in the right OA with a clear poststenotic ﬂ ow pat- tern assumed to origin from the right PCoA via the carotid siphon (ﬂ ow velocity 15/9 cm/s).

occlusion was considered to be the best treatment option and was then successfully performed.

A clinical beneﬁ t of mechanical thrombectomy com- pared with intravenous thrombolysis alone in acute proximal intracranial occlusion of the anterior circulation (distal ICA, M1-MCA, M2-MCA, A1-ACA) was recently conﬁ rmed in ﬁ ve randomized studies including 1,287 patients: MR CLEAN (Berkhemer et al 2015), EXTEND-IA (Campbell et al 2015), ESCAPE (Goyal et al 2015), REVASCAT (Jovin et al 2015), and SWIFTPRIME (Saver et al 2015); for further reading on mechanical recanalization see Case 10, and for technical aspects see Chapter 6, “Technical Aspects of Mechanical Thrombectomy” under “Digital subtraction angiography.” Data focusing on mechanical thrombolysis in patients with CAD and acute artery-to-artery embolic M1-MCA occlusion is scarce and limited to case reports or small observational studies. Successful combined intravenous and intra-arterial thrombolysis followed by thrombectomy in the V3 segment in a patient with bilateral spontaneous VA dissection has been reported (Frankowska et al 2014). A study of 39 patients with high-grade stenosis or occlusion of the cervical ICA and proximal occlusion in the anterior intracranial circulation included 7 patients with CAD, all treated by thrombectomy. Four of them had a good clinical outcome (m-RS 0–2) and no intracranial hemorrhage occurred (Lescher et al 2015). Currently it can be assumed that there is no necessary diﬀ erence in treat- ment approaches between proximal intracranial embolic occlusion in CAD or in atherosclerotic or cardioembolic disorders.

More relevant is the accessibility of the intracranial clot via the dissected artery. Whether a stent should be placed in the extracranial dissected vessel to prevent a permanent vessel occlusion remains an open question. Valid data regarding stent placement in CAD is missing and the risk of dual antiplatelet therapy has to be considered. In our case the dissected ICA occlusion was easily passed by the microcatheter without stenting and the thrombectomy in the MCA was successful. After intracranial thrombectomy was complete, the extracranial ICA

OA-L

Fig. B18.38 TCCS ( tran sorbital a pproach ), lef t-si ded in sona tion. Normalized antegrade ﬂ ow in the left OA (ﬂ ow velocity 31/8 cm/s). Note the diﬀ erent ﬂ ow pattern compared with the initial examina- tion in Fig. B18.18.

Fig. B18.39 Schematic of the patient’s extra- and intracranial brain-supplying arteries after the last duplex ultrasound e x a m i n a t i o n .

remained occluded. The interventionist decided not to place a stent mainly to avoid dual antiplatelet therapy and bleeding into the infarcted parenchyma and because of the decision to start with PTT-guided heparin for secondary embolic stroke prevention. There was no stroke recurrence but increasing dissected stenoses in both V2-VAs and especially in the left-sided distal ICA which resulted in a very critical hemodynamic impairment of both anterior circulations that depended on the collateral ﬂ ow via the PCoAs. Fortunately, no complete vessel occlusion occurred and no hemodynamically related infarction was diagnosed on follow-up brain imaging (for further reading on this complication see Case 11).

Clinically, our left-handed patient suﬀ ered from apha-

sia despite the right-sided territorial MCA infarction. In most people the left hemisphere of the brain is dominant for language and in right-handed subjects the left hemisphere is the speech-dominant side. Left-handed subjects reveal a variety of patterns. Using a word-generation

338 Case 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle

Cerebral Artery Occlusion

task in functional TCD in 326 subjects, right-hemisphere language dominance increased linearly with the degree of left-handedness, from 27% in strong left-handers to 15% in ambidextrous subjects. Interestingly, right-hemisphere language dominance was also seen in 4% of strong right-handers (Knecht et al 2000). These ﬁ ndings were conﬁ rmed by use of the intracarotid amobarbital proce- dure in 174 patients before epilepsy surgery, with a linear increase of right-sided language dominance according to the degree of left-handedness, from 69% in deﬁ nite left-handers and 46% in ambidextrous subjects to 9% in deﬁ nite right-handers (Isaacs et al 2006).

Angiologic and Anatomic Aspects

Duplex sonography is a well-established method of evaluating CAD. Diﬀ erent direct signs visualized by B-mode and color-coded duplex imaging as well as indirect hemodynamic signs assessed by extracranial and intracranial blood ﬂ ow velocity (BFV) measurements exist to diag- nose CAD (for further reading see Case 11). Compared with MRI and conventional angiography a sensitivity of 90% and speciﬁ city of 69% to diagnose cervical ICA dis- section has been reported when considering direct and indirect signs in 70 patients (Alecu et al 2007).

An enormous advantage of ultrasound is its simple use for the serial analysis of cerebral perfusion and embolic activity in highly dynamic processes such as CAD. Signiﬁ cant hemodynamic changes were observed by ultrasound in our patient within 3 months. A stepwise recanalization occurred in the left ICA and both VAs, whereas occlusion persisted in the right ICA. The extracranial reduction of the bilateral VA and left- sided ICA stenoses had a signiﬁ cant eﬀ ect on intracranial collateral pathways. Initially, collaterals for both anterior circulations were assured by both PCoAs and both retrograde OAs. During stepwise recanalization of the left ICA, ﬂ ow in the left OA ﬁ rst turned to an antegrade direction, whereas the collateral ﬂ ow via the PCoA normalized later. This ﬁ nding underlines the

function of the PCoA as ﬁ rst-order collateral in contrast to the OA as secondary collateral. Finally, normalization of ﬂ ow in the left ICA led to a partial cross-ﬂ ow via the ACoA from the left to the right anterior circulation whereas the right MCA remained perfused via the right PCoA. Simultaneously, the right OA collateral ﬂ ow disappeared, indicating that at least in our case a divided collateral ﬂ ow via the ACoA (for the A2-ACA) and PCoA (for the M1-MCA) was the preferential collateral pathway. This case underlines our experience that a markedly activated PCoA might lead to an antegrade ﬂ ow of the OA. This constellation appears rare- ly in solely collateralization via the ACoA (for further reading on collateral ﬂ ow pathways see Chapter 5, “Intracranial Collateral Pathways in ICA Occlusive Processes” under “Collateral Pathways”).

Dissecting aneurysms may be found in about up to 50% of ICA dissections. They persist in 46%, disappear in 36%, and decrease in size in 18%. Usually they do not enlarge and the prognosis is good. Stenting or prolonged oral anticoagulation is not recommended (Guillon et al 1999, Touzé et al 2001). In most cases duplex ultrasound is not able to detect dissecting aneurysms because of their distal location, as was the case in our patient.

Detection of microembolic signals (MES) in CAD—not present in our case—is a second important contribution of ultrasound that cannot be analyzed by other imaging modalities. MES are a frequent ﬁ nding in acute CAD, es- pecially in symptomatic patients presenting with stroke (Ritter et al 2008). In a study of 20 patients with CAD, 17 of them aﬀ ecting the ICA, MES were seen in 25% of them at a rate of up to 15 events per hour. Interestingly, three of these patients presented recurrent cerebral ischemia (Droste et al 2001). In a small study of six patients half of them had MES, all of them with cerebral ischemia. Patients without ischemic event had no MES (Koennecke et al 1997). In acute CAD patients without cerebral ischemia so far, MES have been shown to indicate a higher stroke risk (Molina et al 2000).

(For further reading of the role of other image modalities like MRI, CT, and DSA in CAD see Case 11.)

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