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169Arterial Pathology

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. A5.161 Diﬀ erent quality of collateral blood ﬂ ow via the ACoA in extracranial right ICA occlusion. To p: TOF-MRA, coronal view. Bot- tom: Corresponding Doppler waveform of the MCA ipsilateral to the occlusion. (A) Optimal collateral ﬂ ow with nearly equivalent signals of the MCA including the insular branches and almost normal MCA waveform revealing only a mild elevated diastolic ﬂ ow. (B) Impaired collateral ﬂ ow with an obvious reduced signal in the aﬀ ected MCA (arrows) on the side of the occlusion and a marked poststenotic ﬂ ow pattern in the MCA mainly with an elevated diastolic ﬂ ow but also mild delayed systolic upraise. Note the assumed diﬀ erent diameter of the ACoA explaining the divergent MCA ﬂ ow signals.

A1 A1 A1

ACoA ACoA

stenoses and musical murmurs are frequent ﬁ ndings. In extracranial ICA occlusion, ﬂ ow toward the anterior cir- culation is expected. However, because of the unfavorable insonation angle and the often elongated PCoA course, this is not always evident and a turbulent bidirectional signal may frequently be found. As in ACoA collateral function, the downstream ﬂ ow patterns—normal or poststenotic— depend on the caliber of the PCoA, which varies between

0.5 and 3.3 mm with a mean of 1.2 mm (Lang 2001). If digital tapping of the dominant extracranial VA in V3 at the atlas arch leads to a marked oscillation eﬀ ect within the MCA on the side of the occlusion, a relevant PCoA collateral function can be assumed even if the PCoA itself is not directly accessible. Also, an antegrade ﬂ ow direction of the ipsilateral A1-ACA ensures the presence of a collateral ﬂ ow via the ipsilateral PCoA. Usually, comparable poststenotic ﬂ ow alterations are then seen in the ipsilateral A1-ACA and M1-MCA.

If the A1-ACA on the occlusion side is not accessible despite excellent insonation conditions, both ACA territories are probably supplied by the contralateral A1-ACA which then often shows raised ﬂ ow velocities.

Baumgartner and coworkers (1997a) also performed comparative ultrasound and DSA analyses of the PCoA. An active PCoA collateral was deﬁ ned in case of a PCoA presence with ﬂ ow directed from the P1-PCA to the ICA or raised ﬂ ow velocities within the P1-PCA (>2 SD above the normal systolic blood ﬂ ow velocity). For TCCS they found sensitivity, speciﬁ city, and positive and negative predictive values of 84%, 94%, 94%, and 84%, respectively, which are lower than the corresponding values for for the ACoA collateral. However, it has to be kept in mind that every PCoA visible on DSA is not necessarily a true collateral. Also, lower velocities may be present

BP1 ipsilateralPCoA

Fig. A5.162 Left: Left proximal ICA occlusion. (A) DSA, selective left VA ﬁ lling, posteroanterior view: Collateral ﬂ ow via left PCoA (ar- row) into the left MCA territory (arrows). (B) TCCS, transtemporal approach, axial midbrain plane: Color-mode image demonstrates the PCoA (arrow). Note the short length of the P1-PCA. Right: Corresponding Doppler spectra of the left P1-PCA (raised ﬂ ow velocity without relevant turbulence), the PCoA (raised ﬂ ow velocity and pronounced turbulence), the proximal P2-PCA (normal antegrade ﬂ ow), and the M1-MCA (antegrade ﬂ ow with mild poststenotic ﬂ ow pattern).

Fig. A5.163 Right proximal ICA occlusion. Left: DSA, selective left VA ﬁ lling, lateral view: Collateral ﬂ ow via right PCoA (arrow) into the right MCA territory (arrows). Right: Corresponding Doppler spectra of the right P1-PCA (raised ﬂ ow velocity and turbulence), the right M1-MCA (moderate poststenotic ﬂ ow pattern), and the right A1-ACA (mildly more pronounced poststenotic ﬂ ow pattern but antegrade ﬂ ow). Note, as the ACA ﬂ ow is antegrade, the ACoA and/or left A1-ACA must be hypofunctional. Alternatively, a second ﬂ ow obstruction may be present in the left ICA.

P2 ipsilateral

M1 ipsilateral

P1 ipsilateral

M1 ipsilateral

A1 ipsilateral

in cases with P1 hypoplasia, which explain the lower accuracy of the proposed criteria.

In clinical practice, a mixed collateral ﬂ ow pattern with coexistence of ACoA and PCoA collaterals may be observed with the ACoA mainly providing the blood supply to the ACA territory and the PCoA distributing blood into the MCA territory (Fig. A5.164). Here, a functional stenosis might be detected in both communicating

170 5 Vascular Pathology

PCoA

A1 A2 A2

Fig. A5.164 Patient with combined ACoA and PCoA collateral in right proximal 90% ICA stenosis. (A) 3D TOF-MRA, axial MIP, 90° counterclockwise rotated to correspond with the ultrasound image. Note the strong right PCoA (arrow) and contralateral A1ACA (arrowhead), and the weak intracranial IC A signal (arrows). (B) Corresponding TCCS color-mode image, transtemporal approach, axial midbrain plane (right-sided insonation). Note the strong color signal of the right PCoA.

arteries. Such a “divided” collareral pattern was also seen using arterial spin-labeling MRI in 23 functionally independent patients with symptomatic ICA occlusion, as the MCA ﬂ ow territory ipsilateral to the occluded ICA was mainly supplied by the PCoA, whereas the ACA ﬂ ow territory was mainly supplied by the contralateral ICA via a cross-ﬂ ow (van Laar et al 2007).

Secondary Collaterals (Ophthalmic Artery and Leptomeningeal Collaterals)

Secondary collaterals, i.e., the OA and LMC, will be activated in case of insuﬃ cient primary collateral function (Schneider et al 2015). The OA was long assumed to be a major collateral contributor to cerebral perfusion in ICA occlusion. But considering a mean blood ﬂ ow to be 300 mL/min via a normal ICA and 200 mL/min in a normal MCA, the OA is not able to compensate for this. Studies on extracranial–intracranial (EC–IC) bypass surgery using the superﬁ cial temporal artery as donor vessel showed that an external source of brain perfusion may at best contribute 80 mL/min, which might be the amount the retrograde OA can be responsible for as it receives the blood from similar external sources (Neﬀ et al 2004). Nowadays, OA ﬂ ow reversal is assumed only to occur in case of inadequate or absent communicating artery collaterals.

In the worst instance, the secondary collaterals may be the sole collateral pathways in extracranial vessel occlusion, which usually implies an increased risk of developing hemodynamically related cerebral ischemic infarction (for further details, see Case 11; see also Video A5.16). The orbital collateral ﬂ ow is characterized by a reversed ﬂ ow in the periorbital arteries, visualized using a 4- or 8-MHz Doppler probe, but is best conﬁ rmed by retrograde ﬂ ow in the OA, visualized by a standard tran- scranial 2-MHz sector transducer (Fig. A5.165). In ICA occlusion a reversed OA ﬂ ow can be observed in the ma-

Fig. A5.165 OA collateral in extracranial ICA occlusion. (A) DSA, selective ECA ﬁ lling, enlarged lateral view. Retrograde OA ﬁ lling (small arrows) and blood ﬂ ow into the carotid siphon (large arrow) and distal MCA territory. (B) Corresponding transorbital TCCS, axial plane. Color-mode imaging reveals the blue-coded retrograde OA. Note the brain-supplying OA waveform and the increased ﬂ ow velocities (64/26 cm/s).

jority of patients. Reported incidences by TCD vary between 71% and 77% (Demchuk et al 2000b, Kluytmans et al 1999). Others reported a lower prevalence, e.g., 33% in a mixed patient group of hemodynamic stenoses and occlusions using a 7-MHz linear probe (Nuzzaci et al 1999). On the other hand, a reversed OA ﬂ ow had a speciﬁ city of 100% as has been shown in a TCD study of symptomatic patients with 25 cervical ICA occlusions and 8 near-occlusions (Saqqur et al 2005a). The same speciﬁ city was reported using transorbital duplex sonography in 152 patients (Reynolds et al 2002). If the perfusion pressure is similar within the intra- and extracranial compartments, a watershed phenomenon—zero OA ﬂ ow—may be observed, which means that no OA ﬂ ow is detected by ultrasound. Comparison with the contralateral side will help to diﬀ erentiate between methodologic problems in displaying the OA or a real zero-ﬂ ow constellation. In a duplex sonography study with a 7-MHz linear probe including 112 patients who had a TIA or minor stroke and an ICA stenosis of at least >80% or an ICA occlusion, 33% had a retrograde OA ﬂ ow, 26% revealed a zero OA ﬂ ow, 18% had a reduced ﬂ ow velocity (<25% compared with contralateral OA) but an antegrade ﬂ ow disappear- ing or diminishing during ipsilateral CCA compression. The remaining 23% of patients had an antegrade OA ﬂ ow. N o r e t r o g r a d e o r z e r o O A ﬂ ow was observed in stenoses less than 60% (Nuzzaci et al 1999). Of note, an antegrade OA ﬂ ow may be present even in ICA occlusion, with a re- ported incidence of 26% of cases (Reynolds et al 2002). In these cases the OA ﬁ lling results from at least one of the communicating arteries. Because of the close spatial relationship between OA and PCoA, a predominant OA ﬁ ll- ing via the PCoA collateral pathway can be assumed (Fig. A5.166). Although direct detection of a retrograde OA ﬂ ow is a well-deﬁ ned criterion, in some instances bidi- rectional ﬂ ow may be present. A comparison of ﬂ ow pat- tern between ipsilateral and contralateral helps to decide

171Arterial Pathology

Fig. A5.166 Patient with right proximal ICA occlusion. (A) 3D TOFMRA, coronal MIP. Note the marked right PCoA (arrow) and weak ipsilateral M1-MCA signal intensity indicating hemodynamic impairment (arrows). (B) Corresponding transorbital TCCS, axial plane. Color-mode image and Doppler spectrum reveals an antegrade OA ﬂ ow and an al- most normal OA ﬂ ow pattern (ﬂ ow velocity 27/10 cm/s).

this. An “internalized ﬂ ow” signal—i.e., a pattern with a high diastolic ﬂ ow component—is evidence of retrograde brain-supplying function (Fig. A5.167). An additional tap test may be performed. An orbital collateralization can be assumed if slight digital tapping of the ocular bulb results in a visible oscillation eﬀ ect within the ipsilateral MCA (Fig. A5.168) (Schreiber et al 2006). Instead of the OA, its periorbital peripheral branches, e.g., the supratrochlear artery, may be studied using a continuous-wave Doppler probe. This approach, derived from the early days of clinical ultrasound, is also reliable in collateral assessment of the OA. However, interpretation on direct collateral assessment with the linear or phase-array probe is safer and easier to do, and should be used whenever possible.

LMCs can be indirectly assessed by analyzing blood ﬂ ow velocities in the feeding basal cerebral artery. In ICA occlusion it can be best examined for the PCA. If the P1- and the P2-PCA segments demonstrate equally raised ﬂ ow velocities, LMC seems likely; while a veloc- ity rise solely within the P1-PCA segment indicates a PCoA collateral function (Fig. A5.169). To increase diagnostic certainty, the right and left sides should always be compared, as ﬂ ow velocities in homologous P2-PCA segments are usually similar. A diﬀ erence in velocity of at least 20% between the two P2-PCA segments can be judged as indicative of a LMC ﬂ ow, but ultrasound studies on this topic are rare. A study correlating TCCS and DSA ﬁ ndings regarding LMC from the PCA in occlusive lesions of the carotid artery a P2-PCA peak systolic ﬂ ow velocity >100 cm/s yielded a diagnostic sensitivity of 77% and a speciﬁ city of 83% (Kimura et al 2000).

Using TCD, Müller and Schimrigk (1996) reported LMC activation in patients with ipsilateral steno-occlusive ICA disorders if P2-PCA velocities exceeded the upper range of normal ﬂ ow velocities. In MCA occlusion a LMC ﬂ ow was deﬁ ned by Zanette et al (1995) if an asymmetry index higher than 27% for the ACA and higher than 28% for the PCA was observed (a speciﬁ cation of the exact vessel segment examined was not given).

Fig. A5.167 TCCS, transorbital insonation in a patient with ipsilateral ICA occlusion. (A) Formal antegrade OA ﬂ ow. However, the high ﬂ ow velocity (68/30 cm/s) and a low pulsatility (0.9) are indicative of a brain-supplying artery. (B) Change of sample volume position conﬁ rms the true retrograde OA ﬂ ow toward the brain. The phenom- enon is easily explained by a frequently observed OA elongation.

Fig. A5.168 Patient with isolated OA collateral in left proximal ICA occlusion. (A) 3D TOF-MRA, coronal MIP. Note the strong right OA (arrow) and weak ipsilateral M1-MCA signal intensity (arrows). (B) Digital tapping of the eyeball. (C) Corresponding TCCS colormode image and Doppler spectrum, transtemporal approach, axial midbrain plane. Note the strong oscillation eﬀ ect on the M1-MCA and the marked poststenotic ﬂ ow pattern of the MCA. (D) Corre- sponding TCCS, color-mode image and Doppler spectrum, transtemporal approach, upper pontine plane. Note the blue-coded (retrograde) OA ﬂ ow and the marked response on eyeball tapping.

Others deﬁ ned an increased P2-PCA mean ﬂ ow velocity >30% compared with the analogous contralateral side as LMC (Kim et al 2006). A recent TCCS study in 68 patients with symptomatic ICA occlusion used the latter threshold and reported a higher rate of PCA ﬂ ow activation in patients with recurrent symptoms than in patients with stable disease indicating that adequate primary collaterals were not present (Schneider et al 2015). Flow velocity diﬀ erences >30% have also been reported in the ACA in extracranial diseases (Müller and Schimrigk

1996) and intracranial steno-occlusive disorders (Kaps

172 5 Vascular Pathology

Fig. A5.169 PCA leptomeningeal collateral ﬂ ow in the left proxi- mal ICA occlusion. (A) 3D TOF-MRA, coronal MIP. Note the marked left PCA (arrow) indicating leptomeningeal collateral ﬂ ow. (B) Cor- responding TCCS, color-mode, axial midbrain plane. Note the ﬂ ow velocities at the P1/P2-PCA border (141/69 cm/s). (C) Corresponding TCCS, color-mode, axial thalamic plane and at the P2/P3-PCA transition (110/46 cm/s). The increases ﬂ ow velocities in all main segments of the PCA indicate LMC ﬂ ow via the PCA.

et al 1990, Y.S. Kim et al 2006). Because of the variable diameter of the A1-ACA, however, measured ﬂ ow veloc- ities should be considered cautiously. When using TCCS, variable angles of A2-ACA insonation have to be kept in mind and angle correction should be used if possible. In good insonation conditions even cortical branches, especially of the PCA, may be detected and their ﬂ ow velocity and therefore their possible involvement in PCA LMC can be assessed (Fig. A5.170 and Fig. A5.171). Ve- locities higher than two SD above normal ﬁ ndings may be used to indicate activation in PCA branches (see also

Tab le A2.3 ).

Table A5.2 summarizes the possible intracranial col-

lateral patterns in extracranial ICA steno-occlusive disorder of ≤70% stenosis (NASCET criteria) and their main ultrasound criteria (Table A5.2). Not all features may be present, but conﬁ dence increases if several criteria are detected. In poor examination conditions, transients in the ipsilateral M1-MCA waveform during digital tapping of the contralateral submandibular ICA, the dominant V3VA at the atlas arch, and/or the ocular bulb may further help to identify the collateral pathways.

Intracranial Collateral Pathways in VA Occlusive Processes

In contrast to unilateral occlusive processes of the ICA, a severe unilateral extracranial VA stenosis or occlusion only rarely leads to a compromised intracranial hemodynamic constellation. This is mainly caused by the anatomic constellation of both VA merging into the BA. In proximal VA occlusion the PICA, originating from the distal intracranial VA, is often supplied by the contralateral VA in a vertebro-vertebral overﬂ ow pattern (for further details, see “VA Occlusion” under “Intracranial Pathology” above). Intracranial collateral activation is required if both VAs are functionally impaired by a bilateral steno-occlusive disorder, in cases

Fig. A5.170 Leptomeningeal collateral ﬂ ow via PCA branches in left extracranial ICA occlusion. (A) DSA, selective right VA ﬁ lling, posteroanterior view. Collateral ﬁ lling of the left MCA territo- ry via a prominent occipitotemporal artery (arrow). (B,C) TCCS color-mode image, axial midbrain plane and corresponding Doppler spectra demonstrating a marked vessel signal of the o c c i p i t o t e m p o r a l a r t e r y P C A b r a n c h w i t h i n c r e a s e d ﬂ ow velocities (92/31 cm/s).

Fig. A5.171 Left-sided proximal ICA and MCA occlusion. (A) 3D TOF-MRA, axial MIP. Note the marked left PCA (arrows) indicating leptomeningeal collateral ﬂ ow. No MCA signal is visible. (B–D) TCCS, axial midbrain plane and corresponding Doppler spectra. Note the increased ﬂ ow velocities in the proximal P2-PCA (116/48 cm/s) (A), anterior temporal artery (71/31 cm/s) (B), and the occipitotemporal artery (68/30 cm/s) (C), indicating LMC via PCA main stem and its cortical branches.

with unilateral VA occlusion and contralateral hypoplasia (incidence of unilateral hypoplasia in ~10%), or in unilateral occlusion and contralateral VA terminating as the PICA. In the worst case scenario, the total posterior circulation, the cerebellum, and brainstem are supplied via the anterior circulation by one or both PCoAs, which requires retrograde BA and VA ﬂ ow (Fig. A5.172). Alternatively, LMC starting from the PICA could bypass the occlusion by ﬁ lling up the SCA (Fig. A5.173). The main limiting factor for this collateral pattern may be bilaterally nonfunctional PCoAs, which, however, are found only in ≤16% of cases (Hoksbergen et al 2000b). For further reading see also Case 35 and Case 41.

173Arterial Pathology

Tab le A5. 2 Synopsi s of intracranial collatera l pathways in extra cranial ICA occlusion or >70–80% stenosis

Via ACoA Via PCoA

Ipsilateral M1 (↓) Ipsilat

Ipsilateral retrograde A1 Ipsilateral P1 ↑

Functional stenosis ACoA Ipsilateral P2 normal

Contralateral A1 ↑ Functional stenosis PCoA

Contralateral A1 > M1 Ipsilateral A1 antegrade with

Via LMC Via OA

Ipsilateral P2 = P1↑ R

PCA branches ↑

↑ Flow velocity increased. ↓ Flow velocity decreased.

eral M1 (↓)

ﬂ ow pattern similar to ipsilateral M1

etrog

rade or zero OA ﬂ ow

PCA

SCA

Occlusion

PICA

Fig. A5.173 (A) Schematic demonstrating a collateral ﬂ ow pattern in proximal BA occlusion. Note that the occlusion can be bypassed through LMC connecting the PICA with the SCA. The distal BA is perfused retrogradely by the SCA or by one or both PCoAs (adapted from Zülch 1985). (B) DSA, selective VA injection, lateral view in a patient with a proximal BA occlusion (arrow). Note the collateral ﬂ ow from the PICA (arrowhead) to the cortical branches of the SCA (curved arrow) and from there to the distal BA (dotted arrow).

also able to function in reverse in CCA or BCT occlusion and to ﬁ ll the ICA via the retrograde ECA (for further details, see “CCA Stenosis and Occlusion” and “Brachiocephalic Trunk Stenosis,” both under “Extracranial Pathology” earlier in this chapter). Other, less common, collateral patterns are a VA ﬁ lling via the ladder-like spinal arteries from the con- tralateral VA (for further details, see “VA Occlusion” under “Extracranial Pathology” above). The very rare collaterals from ICA to the BA via persisting primitive embryonic vessels are quantitatively irrelevant.

Fig. A5.172 DSA, selective ICA injection, lateral view in a patient with bilateral extracranial VA occlusion. (A) Retrograde BA ﬁ lling (arrows) via a PCoA (arrowhead). (B) Late arterial phase—retrograde BA ﬁ lling extends down to one VA (arrows) and from there into the PICA (arrow). Note that the precondition of this ﬂ ow pattern is an intact PCoA. However, the PCoA is not clearly visible, although it has to be present and functional.

Alternatively, LMC starting from the PICA could bypass the occlusion by ﬁ lling up the SCA (Rhoton 2000) (Fig. A5.173).

Extracranial Collateral Pathways in VA Occlusive Processes

Extracranial collateral pathways may also be activated to assure suﬃ cient intracranial perfusion. This may occur es- pecially within the VA, which in contrast with the ICA often anastomoses with primarily non-brain-supplying arteries, even under physiologic conditions. In hemodynamically relevant occlusive VA processes several collateral patterns can be observed that result in a secondary, post-occlusive VA ﬁ lling (for further details, see “VA Occlusion” under “Ex- tracranial Pathology” above). Frequently, distal ﬁ lling at the distal V2-VA or the level of the atlas loop via the thyrocervical trunk anastomoses and ECA branches, especially the occipital artery, can be observed. The latter anastomosis is

Clinical Relevance of Collateral Pathways

Although current scientiﬁ c interest is focuses mainly on all aspects of revascularization, there is growing awareness of the importance of collateral pathways, particularly as suﬃ cient collaterals may prevent the occurrence of stroke or at least alleviate the severity of damage (Liebeskind et al 2011, Miteﬀ et al 2009). In the acute

e setting the maintenance of collateral pathways is

rok

t as important as therapeutic recanalization. In the

at leas chronic phase, the quality of the collaterals substantially determines the patient’s prognosis.

Extracranial Occlusive Processes

Data on collateral-dependent clinical prognosis in patients with symptomatic extracranial ICA stenosis have been reported from the NASCET trial. DSA images were analyzed for the presence of an ACoA, PCoA, and OA collaterals, omitting the LMCs for methodologic reasons (Henderson et al

2000). In 280 patients DSA revealed collateral pathways. A singular collateral ﬂ ow via the ACoA was found in 69.7% of cases, an exclusively PCoA collateral in 8.9%, an exclusively OA collateral in 1 .8%, and a mixed patter n in 1 9.7%. The existence of collaterals correlated as expected with the degree of stenosis. Collateral blood ﬂ ow was found in 63.6% of near- occlusions, in 42.7% of 85–99% stenosis (NASCET criteria), in

174 5 Vascular Pathology

25.3% of 70–84% stenosis, in 3.1% of 50–69% stenosis, and in 0.5% of stenoses <50%. In the medically treated patients the stroke risk signiﬁ cantly increased with the increasing degree of stenosis except for the near-occlusions. If collaterals were present, patients with stenoses between 70–84% and 85–99% had a two-thirds reduced risk of stroke. If the 7 0 – 9 9 % s t e n o s e s w e r e c o m b i n e d , t h e 2 - y e a r r i s k o f h e m i spheric stroke with collaterals present was signiﬁ cantly reduced (11.3% versus 27.8% for absent collaterals). The likelihood of a TIA (19.1% versus 36.1%) or a disabling stroke or fatal stroke was also signiﬁ cantly reduced (6.3% versus

13.3%). In the operated patients, the presence of collaterals resulted in a reduced perioperative risk (1.1% versus 4.9%) and a lower 2-year risk of hemispheric stroke (5.9% versus

8.4%), although neither diﬀ erence reached statistical signiﬁ - cance (Henderson et al 2000).

With regard to the development of border zone infarction

(BZI), collateral ﬂ ow via the PCoA seems to have a protective eﬀ ect. In a patient group of 51 patients with extracranial ICA occlusion and <70% contralateral ICA stenosis, the incidence of PCoA collaterals was 50% in those without a BZI compared with 12% in those with BZI. Patients without BZI also revealed signiﬁ cantly larger PCoA diameters (1.6 mm versus

1.3 mm). On the other hand, a cross-ﬂ ow via the ACoA was not protective as a comparable prevalence was seen in both groups (60% versus 69%) (Hendrikse et al 2001).

The quality of the collaterals may also be evaluated indirectly by measuring the cerebrovascular reactivity (CVR). In a TCD study of 85 patients with asymptomatic ICA occlusion followed over 38 ± 15 months, only 8% of patients with normal CVR developed a TIA and no strokes occurred. In contrast, 32% of patients with diminished or exhausted CVR had a TIA or completed stroke (Kleiser and Widder

1992). Exhausted CVR determined by a Doppler CO the MCA ipsilateral to the stenosis was the only signiﬁ cant

test in

independent predictive parameter for disabling stroke in 104 consecutive patients with symptomatic severe carotid artery stenosis before carotid endarterectomy (odds ratio [OR], 9.7; 95% conﬁ dence interval [CI], 2.1–44.1) (Blaser et al 2002). The occurrence of secondary collaterals is also suggestive for an insuﬃ cient collateral blood supply. A TCD study of 25 patients with asymptomatic extracranial ICA occlusion demonstrated signiﬁ cantly lower systolic MCA ﬂ ow velocities on the side of the occlusion (55 ± 22 cm/s versus 79 ± 24 cm/s). Furthermore, a retrograde OA ﬂ ow was asso- ciated with a low MCA ﬂ ow velocity and with the absence of primary collaterals (Schneider et al 1991). This was further conﬁ rmed by a combined TCD and DSA study in 70 patients with ICA occlusion and minor stroke. In these patients, a retrograde OA ﬂ ow or activation of LMC was associated with a signiﬁ cant impairment of CO compared with patients with exclusively primary collaterals

CVR (8 ± 14% versus 33 ± 18%)

such as the ACoA and PCoA (Hofmeijer et al 2002). A recently published meta-analysis including 754 patients in 9 studies conﬁ rmed that a restricted CVR may indicate a higher risk of stroke. In a multiple regression model, impaired CO reactivity was independently associated with an increased risk of ipsilateral ischemic stroke (hazard ratio [HR] 3.69; CI 2.01, 6.77; p < 0.0001). Interestingly, risk prediction was similar for recently symptomatic versus asymptomatic patients (Reinhard et al 2014).

Intracranial Occlusive Processes

In intracranial occlusions, the LMCs are the only collateral blood supply. In these circumstances their activation does not reﬂ ect insuﬃ cient collateralization but is the only opportunity to reduce the extent of impaired perfusion. In a study of 97 intra-arterial and 14 intravenously thrombolyzed patients with intracranial occlusions of the anterior circulation, multivariate analysis revealed that the most important factor for the clinical outcome was the existence of well-developed LMCs (OR 5.9, CI

1.3–26.7) which was deﬁ ned as retrograde ﬁ lling of at least three MCA branches up to the M2 segments and no successful recanalization (OR 1.9, CI 0.5–6.6) (Kucinski et al 2003). In a comparable study of 53 stroke patients the LMC quality also signiﬁ cantly correlated with infarct volume and clinical outcome, independent of the extent of the recanalization achieved (Christoforidis et al 2005, Higashida et al 2003). Using CTA (Frölich et al 2014, Lima et al 2010, Maas et al 2009, Miteﬀ et al 2009) and MRA (Bang et al 2008b, Ichijo et al 2013, K.Y. Lee et al 2009) it was further conﬁ rmed that the eﬃ cacy of LMC deter- mines long-term functional outcome in stroke patients with large intracranial vessel occlusion. More recently, CTA and DSA-based studies showed that a patient with good LMC beneﬁ ts more from intra-arterial recanali- zation treatment than a patient with poor collaterals (Liebeskind et al 2015, Nambiar et al 2014).

The function of LMC in MCA occlusion can be assessed by ultrasound techniques by detection of raised ﬂ ow veloc- ities within the ACA and PCA, also called ﬂ ow diversion. In a group of 47 patients with persisting M1-MCA occlusion after rt-PA thrombolysis, only those patients presenting with a ﬂ ow diversion improved clinically: 90 minutes after rt-PA bolus, 22% with and 0.52% without ﬂ ow diversion had clinically improved. Twenty-four hours later, patients with collaterals remained stable (29%) whereas patients without LMCs had worsened (−25%) (Y.S. Kim et al 2006). These data indicate that the quality of LMCs may determine the time window for thrombolysis and thrombectomy.

Very little data is available for the role of collateral ﬂ ow in posterior circulation stroke. In an angiographic study of 51 patients with BA occlusion, factors inﬂ uencing out- come, in addition to vessel recanalization, were the initial clinical condition, the length of the BA occlusion, and the status of collateral supply (Brandt et al 1996). Also, a retrograde collateral ﬂ ow within the distal BA was associat- ed with better clinical outcomes in proximal BA occlusion (Ribo et al 2004).

Role of Blood Pressure and Other Approaches to Augmentation of Cerebral Blood Flow

The role of blood pressure in acute intracranial vessel occlusion is still controversial although elevated blood pressure is considered to facilitate collateral ﬂ ow. Normally, cere- bral blood ﬂ ow (CBF) is independent of the systemic blood

pressure within a wide range due to autoregulatory mechanisms (for further reading, see Chapter 3, “Autoregulation”). Within the ischemic area autoregulation is impaired, so it can be assumed that brain perfusion is directly dependent on blood pressure in both directions. A therapeutic increase

175Venous Pathology

of blood pressure might therefore improve brain perfusion and reduce the extent of the ischemic area. Clinical observations seem to support this assumption. Reduction of blood pressure within the ﬁ rst 24 hours after stroke was related to a poor clinical outcome after 3 months (Oliveira-Filho et al 2003). The level of systolic blood pressure after acute ischemic stroke was found to be inversely related to the degree of vessel recanalization. A sudden drop in blood pressure may therefore indicate achieved recanalization, and patients without recanalization remained hypertensive for longer time periods than those with successful recanalization (Mattle et al 2005). Following this observation several groups started to treat ischemic stroke patients with a drug-induced hypertension. A small clinical study analyzed the clinical outcome of 13 patients who received phenylephrine to increase blood pressure by 20% or up to 200 mm Hg outside the time window for thrombolysis. Seven of them demonstrated clinical improvement by two points on the National Institutes of Health Stroke Scale (NIHSS) scale without the occurrence of any complication (Rordorf et al

2001). A further step was taken in a second pilot study in which serial MRI perfusion/diﬀ usion images were also ob- tained. They used intravenous phenylephrine, leading to a 10–20% increase in mean arterial pressure (MAP) over the course of 1–8 hours or to a 10% increment until motor or cognitive deﬁ cits improved or a MAP of 130–140 mm Hg was achieved. The ﬁ nal MAP was maintained for at least 24 hours. A signiﬁ cant clinical improvement was shown only in the group with medically raised blood pressure. Correspondingly, MRI demonstrated a signiﬁ cant reduction of the hypoperfused brain regions and a reduction of the mismatch area in comparison with the untreated group (Hillis et al 2003). A similar approach was used in a case series of six patients with acute hemodynamic stroke and blood pressure-dependent clinical ﬂ uctuation of neurologic symp- toms by means of TCCS and pharmacologically induced hypertension. They showed that a catecholamine-induced hypertension led to an ultrasound-detectable rise of cerebral blood ﬂ ow velocity and amelioration of NIHSS severity (List et al 2013) (Fig. A5.174). Deterioration may also occur in a hemodynamically compromised cerebral perfusion when the administration of acetazolamide or a CO to decreasing ﬂ ow velocities in the aﬀ ected M1-MCA, also

test led

called a reversed Robin Hood eﬀ ect (Alexandrov et al 2007, Palazzo et al 2010, Sharma et al 2011).

Currently, indirect interventions to increase CBF in the ischemic area, in addition to drug- or volume-induced arterial hypertension, are the partial aortic occlusion approach which has been shown to increase ﬂ ow velocities measured by TCD in patients with good outcome (Saqqur et al 2013), and external counterpulsation, which apparently does not inﬂ uence blood ﬂ ow velocities (W. Lin et al 2012, 2014). Finally, extracranial–intracranial bypass surgery is one way to ameliorate CBF (for further reading on EC–IC bypass see Case 9).

Venous Pathology

Cerebral Venous Thrombosis

Cerebral venous thrombosis (CVT) is the most important venous-related brain disease. Like the arterial

M1-MCA

OTA-PCA

Fig. A5.174 Example of intracranial blood pressure-dependent

ﬂ ow velocity changes. Top: M1-MCA. Bottom: OTA (occipitotempo- ral artery, cortical PCA branch). Doppler sample volume is marked by red circles. The white dotted lines indicate the location of the midbrain. The individual ﬂ ow velocities at the corresponding blood pressure values were for the MCA (top): 125 mm Hg–28/21 cm/s; 150 mm Hg–39/26 cm/s; 165 mm Hg–45/26 cm/s and for the OTA (bottom): 100 mm Hg–81/31 cm/s; 125 mm Hg–96/38 cm/s; 150 mm Hg–119/46 cm/s. (Reproduced from List et al 2013.)

vascular system, venous vessels and venous ﬂ ow pa- thology can be studied by ultrasound techniques. TCD has been used for detecting venous collateral pathways in CVT (Canhão et al 1998, Valdueza et al 1995, Wardlaw et al 1994). But, as in arterial stroke, TCCS oﬀ ers clear advantages due to its better anatomic orientation in the assessment of venous vessel anatomy (Becker et al 1995, Ries et al 1997, Stolz et al 2002a). Direct thrombus visualization is not possible but, similar to the use of ultrasound in deep venous thrombosis of the legs, collateral pathways can be assessed and monitored (Stolz et al 2002a, Valdueza et al 1999a). Because of the absence of valves in the intracranial venous system, ﬂ ow 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 ﬂ ow determine whether or not an increase in velocity occurs, which can subsequently be detected by ultrasound (for further reading on venous anatomy and TCCS examination of veins and sinuses, see also “General Venous Anatomy” in Chapter 2 and Case 29).

Diﬀ erent collateral drainage patterns can be observed

in CVT, depending on the location of the thrombus.

Superior Sagittal Sinus Occlusion

An interruption of ﬂ ow in the superior sagittal sinus (SSS) may be compensated by major collateral veins on the lateral surface of the brain, which are eﬀ ectively connected to one another and to the principal venous outlets. Depending on the site of the occlusion and the pre-existing venous anatomy, venous blood is collected by sylvian veins draining into the sphenoparietal sinus (SpPS) and cavernous sinus (CS), or by the inferior anastomotic vein (vein of Labbé) draining to the transverse sinus (TS). The blood may also run to the internal cerebral vein (ICV) and the BVR

176 5 Vascular Pathology

through transcerebral anastomoses and from there to the straight sinus (StS) and the TS (see also Video

A5.17).

Deep Cerebral Venous System Occlusion

In occlusion of the vein of Galen (VG) or the StS, the BVR becomes an important collateral vessel (as long as the BVR is not aﬀ ected itself) with ﬂ ow reversal and blood distri- bution into two main pathways: via the lateral mesencephalic vein to the petrosal vein and superior petrosal sinus, and through the deep middle cerebral vein (DMCV) to the sylvian veins, the SpPS, and CS. The blood may also run to the SSS through transcerebral anastomoses, which connect the deep cerebral venous system with the superﬁ cial veins.

Lateral Sinus (Transverse and Sigmoid Sinus) Occlusion

Variations of the lateral sinuses are common and of great importance in understanding hemodynamic changes in CVT. A complete separation between the SSS and StS drainage is present in ~10%. If this is the case, a TS occlusion may lead either to symptoms of StS or to SSS occlusion. If only the sigmoid sinus (SiS) is aﬀ ected, ﬂ ow in the ipsilateral TS will be reversed, caused by inﬂ ow from the vein of Labbé and other vessels merging into the TS.

Based on the above collateral pathways, six ultrasound

constellations can be diﬀ erentiated which can be found alone or in combination in ~70% of CVT patients.

Fig. A5.175 (A) Intracranial CTA, axial MIP. Lack of contrast enhancement within the posterior part of the superior sagittal sinus (arrow) and mainly left transverse sinus (arrowhead). (B,C) Corresponding TCCS, color-mode and Doppler spectrum, axial upper pontine plane. Note the increased ﬂ ow velocities in the sphe- noparietal sinus (57/36 cm/s) indicating collateral ﬂ ow. Note also the carotid siphon (arrow) conﬁ rming the correct insonation plane.

Flow Abnormalities in Cerebral Venous Thrombosis

Absent Flow Signals

Because of the known anatomic variation of intracranial venous vessels, absence of a ﬂ ow signal might represent hypoplasia or aplasia, impaired insonation conditions, or thrombosis. In suspected TS thrombosis several authors have found that absent ﬂ ow on TCCS does not cor- relate well with a vessel occlusion. Even echo ce-TCCS has frequently failed to detect aplasia and hypoplasia as well as 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 ﬂ ow velocities may indicate venous stenosis dur- ing gradual recanalization (Stolz et al 1999a).

Pathologic Diﬀ erences Between the Right and Left Sides

In healthy subjects, bilateral diﬀ erences >50% are usually not observed in the BVR and DMCV, in contrast to the other paired venous vessels. In CVT they often persist even over longer periods of time and might indicate partial recanalization. In TS thrombosis a compensatory increase in ﬂ ow in the contralateral TS can frequently be observed (Stolz et al 1999a, 2002a). As symmetric TSs are present in only ~25% of cases, asymmetric ﬂ ow velocities within the TS should be considered carefully.

Increased Flow Velocities

Raised ﬂ ow velocities in venous collaterals are the most frequent ﬁ nding in CVT (Fig. A5.175). If increased ﬂ ow

Fig. A5.176 (A) Intracranial CTA, sagittal MIP. Note the ﬁ lling defect in the vein of Galen (arrow), probably representing an arachnoid (Pacchionian) granulation. (B) Intracranial CTA, axial MIP, revealing a lumen narrowing at the junction of the vein of Galen and the straight sinus (arrow). (C,D) Corresponding TCCS to A, color-mode and Doppler spectrum, axial thalamic plane. Note the ﬂ ow turbulence and increased velocities in the vein of Galen (71/42 cm/s) assumed to present a physiologic variant.

velocities are detected, they are highly suspicious for an underlying CVT; however a variety of pitfalls must be considered. Increased ﬂ ow velocities may be detected in the inﬂ ow (SpPS) and outﬂ ow (SPS) region of the CS (Valdueza et al 1998). If present, they do not reﬂ ect venous pathology but are rather caused by physiologic venous narrowing at the entrance and exit points of the CS. Physiologically raised ﬂ ow can also be observed in the proximal StS in a high number of cases (Fig. A5.176) (Schreiber et al 2012). It may also be observed in the TS if large arachnoid (Pacchionian) granulations cause venous vessel narrowing. Finally, increased velocities may be detected in CVT in partially recanalized sinuses. Raised venous velocities may, however, be observed in arteriovenous malformations (AVMs) or dural ﬁ stulas

177Venous Pathology

Fig. A5.177 (A) Intracranial venous MRA, sagittal MIP. Note the irreg- ular ﬁ lling defects in the midpart of the superior sagittal sinus (arrows) and the transverse sinuses (arrowheads) in severe CVT. An important collateral ﬂ ow runs from the distal superior sagittal sinus retrograde via the straight sinus and the vein of Galen mainly into the internal cerebral vein (red arrow) and basal vein of Rosenthal. (B,C) Corresponding TCCS , colo r-mo de an d Dopp ler s pect rum , axia l thal amic plan e. Note the retrograde ﬂ ow in the basal vein of Rosenthal (17/14 cm/s).

(Harrer et al 2005) and in generalized or local hyperemia. The latter can be observed in herpes simplex virus encephalitis and also after subarachnoid hemorrhage (Doepp et al 2006, 2009).

Reversed Venous Flow Direction

A reversed BVR ﬂ ow is a frequent ﬁ nding in StS occlusion (Baumgartner et al 1997b, Stolz et al 2002a, Valdueza et al 1999a). In these cases the BVR mainly serves as collateral for blood deriving from the inferior sagittal sinus, VG, and ICV, draining into the SpPS or CS. It may also be seen in bilateral obstruction of the TS (Fig. A5.177). A retrograde ﬂ ow may also be detected in the proximal part of the TS if an occlusion exists distal to the vein of Labbé (Fig. A5.178) (Stolz et al 2002a).

Reduced Venous Blood Volume Flow

Reduced venous blood volume ﬂ ow (BVF) in the inter- nal jugular vein (IJV) was described in a group of 40 CVT patients diagnosed by MRI. In patients with unilateral disease (SiS and/or TS) the mean BVF was 53 ± 31 mL/min (range 0–96 mL/min) whereas controls had a mean BVF of 435 ± 137 mL/min. Signiﬁ cantly lower BVF values compared with controls have also been reported in patients with more generalized CVT conditions (Özen et al 2014).

Venous High Intensity Transient Signals

Venous microembolic signals (MES) can be observed in the outﬂ ow vessels of patients with CVT (Fig.

A5.179). In a study

of six patients with SSS thrombosis, half of them showed MES in the venous outﬂ ow vessels. In the control group MES were not observed. They are thought to be related to the fragmentation of proximally located thrombotic material. The rate of MES and the duration of their occurrence,

Fig. A5.178 Left: Middle: DSA, left VA injection, posteroanterior view. Note the occlusion of the left proximal sigmoid sinus (arrow). Top : Corresponding TCCS, color-mode and Doppler spectrum, upper pontine plane, insonation from the left side. Note a normal antegrade ﬂ ow in the right transverse sinus (22/13 cm/s). Bottom: Corresponding TCCS, color-mode and Doppler spectrum, upper pontine plane, insonation from the right side. Left transverse sinus with retrograde ﬂ ow (16/10 cm/s) caused by the obstruction of the left sigmoid sinus.

Fig. A5.179 Spontaneous venous microembolic signals in a patient with CVT. TCD, transforaminal approach insonation at 88 mm depth with detection of the inferior petrosal sinus above the zero line and of the BA below the zero line. Note three venous microembolic signals.

however, varied greatly. MES were found ranging from 3 to 150 per 15 minutes. The emboli subsided during high-dose heparin in 2 patients after 2 and 11 days, respectively. In a third patient MES were detected even after 110 days. No pulmonary embolism occurred, so their clinical signiﬁ cance is yet unclear (Valdueza et al 1997). Similar ﬁ ndings were reports in patients evaluated with duplex ultrasound of the superﬁ cial femoral vein for DVT. Here 60 of 218 patients studied demonstrated MES with a range from 5 to 800 HITS per minute. Heparin decreased the embolus counts of more than 50% within 24 hours, and all MES were abolished within 72 hours (Nicholls et al 1996).

In ~30% of cases with CVT, no pathologic sonographic signs can be detected. Therefore, normal TCD and/or TCCS do not exclude a CVT. Ultrasound cannot replace CTA or

178 5 Vascular Pathology

MRA as primary diagnostic tool, but may be used as a complementary 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 ﬂ ow signals. High initial venous ﬂ ow velocities correlate with altered consciousness (Valdueza et al 1999a) while patients with initially normal venous ﬂ ow signals or ﬂ ow normaliza- tion within 90 days demonstrate a signiﬁ cantly better clinical outcome (Stolz et al 2002a).

Ultrasonography of the Internal Jugular Vein in Intensive Care Patients

Central Venous Cannulation

Duplex ultrasound is a reliable technique to facilitate catheter placement in the IJV (Teismann et al 2013b). It reduces the risk for failed catheter placement and for complications during IJV cannulation (Hind et al 2003). Duplex ultrasound is helpful to exclude IJV thrombosis before cannulation, and to detect catheter-related thrombosis and infection (Lordick et al 2003). As venous drainage patterns vary, e.g., 70% of individuals have a right-sided dominant IJV, ultrasound also helps to detect these variations and to select the preferable side and optimal degree of head rotation for venous puncture (Lamperti et al 2012, Lichtenstein et al 2001). Either a longitudinal or a transverse ultrasound approach minimizes the risk of catheter misplacement into the CCA or other deep cervical veins, for instance the VV (Ide et al 2012) (Fig. A5.180). The IJV reaches the maximal dilation in a head-tilt maneuver within a few seconds and therefore discomfort for the patient can be minimized (Schreiber et al 2002b). Drainage via the IJVs is not signiﬁ - cantly altered after ultrasound-guided cannulation, which is important to know in patients at risk of raised intracranial pressure (Vailati et al 2012).

Fig. A5.180 Ultrasound-guided jugular vein puncture. (A) Needle and ultrasound probe positioning for “in plane” needle insonation. (B–D) Continuous visualization of the needle (arrows) during stepwise advancement. (D) Successful placement of the needle tip in the venous lumen (arrow).

since the introduction of TCBS several pathologic conditions aﬀ ecting intracranial brain structures have been described.

Indirect Assessment of Central Venous Pressure (CVP)

The cross-sectional area (CSA) of the IJV increases with the CVP. An end-expiratory diameter of the right IJV <10 mm measured 2 cm above the level of the clavicle in a supine position seems reliable in excluding an elevated CVP >10 cm

O (Donahue et al 2009). In case of increased CVP the Val-

salva maneuver (VM) has less eﬀ ect on the CSA of the IJV. A VM-induced CSA increase >17% in the right IJV makes an elevated C VP ver y unlikely (Simon et al 2010).

Intracranial Stroke-related B-mode Pathology

Compared with the extracranial assessment of B-mode images using ultrasound probes of at least 7 MHz, the intracranial approach has the disadvantage of the 1–2-MHz low insonation frequencies and the sector probe conﬁ guration that have to be used for skull penetration in transcranial B-mode sonography (TCBS). This results in a lower spatial resolution of the ultrasound images, which subsequently limits the potential diagnostic value. For instance analysis of atherosclerotic vessel wall changes or vessel diameter measurements is not possible with this approach. However,

Ventricles

Early reports about ultrasound assessment of intracranial structures go back to the 1970s, when normal values of the lateral ventricles were reported in a group of 25 normal and 41 high-risk infants (Johnson et al 1979). A description of the transcranial visualization of brain parenchymal structures like the midbrain, thalamus, or lateral ventricle in adults followed only some years later (Becker et al 1991, Bogdahn et al 1990). In 1995 Seidel and coworkers published a study with data on normal values for the third and the lateral ventricles. Individuals up to 59 years of age had a diameter of 4.8 ± 1.9 mm and 16.7 ± 2.3 mm for the third ventricle and the lateral ventricle, individuals from 60 years onwards diameters of 7.6 ± 2.1 mm and 19.0 ± 2.9 mm, respectively. In addition, the authors correlated CT and TCBS data and found a signiﬁ cant correlation for the measure- ments of the third and the lateral ventricles. Similar values for the diameter of the third ventricle and lateral ventricle in a group of 12 healthy individuals with a mean age of 46 years, 5.2 ± 1.6 mm and 16.5 ± 2 mm, respectively, were reported in the same year by others (Seidel et al 1995). Generally, the intra- and interobserver reproducibility is reported to be high. On comparison of normal B-mode insonation and the use of tissue harmonic imaging, the latter seems to yield the better results (Puls et al 1999).

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