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379Discussion

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.

origin. Usually in such cases, collaterals from the ICA via one or both PCoAs to the PCA, and if necessary to the BA, compensate for this deﬁ cit. Patients with this ﬂ ow pattern are considered to be at high risk of subsequent ischemic stroke (de Bray et al 1994, Grosset et al 1992). In our patient, however, even this type of collateral ﬂ ow was not possible because of bilateral lack of functional PCoAs, a variation of the cerebral arterial circle (circle of Willis) which is present in ~16% of the population (Hoksbergen et al 2000b). The coexistence of bilateral

nonfunctional PCoAs and bilaterally impaired VA ﬂ ow explains the distinctly poststenotic altered ﬂ ow pattern in both PCAs, which hardly demonstrated any arterial pulsatility. It also explains why both PCAs appeared extremely small on DSA, which could have been interpreted as part of the arteritis even though involvement of the intracranial arteries is extremely rare in TA (Nasu

1975). After successful bypass surgery, both PCA ﬂ ow proﬁ les normalized, arguing against the hypothesis of an additional vasculitic PCA involvement.

380

Case 24

Dissection of the Right Extracranial Internal Carotid Artery and Left M1 Middle Cerebral Artery

Clinical Presentation

A 34-year-old woman presented with a 1-year history of severe headaches that were thought to be caused by repeated hypertensive episodes. She also reported a single episode of left-sided facial pain and ipsilateral conjunctival injection lasting for several hours ~1 year ago. After the initiation of antihypertensive treatment the headaches subsided. However, ambulatory examination of the optic fundi revealed retinal vessel narrowing. This ﬁ nding prompted an ultrasound examination of the brain-supplying arteries. Transcranial Doppler (TCD) revealed a left M1 middle cerebral artery (MCA) stenosis. In addition to having hypertension, the patient was a smoker and used an oral contraceptive. An ambulatory cerebral CT scan had been unremarkable. She was now admitted to our department for elective catheter angiography to search for extended intracranial vascular pathology.

Initial Neuroradiologic Findings

Digital subtraction angiography (DSA) demonstrated mild bilateral extracranial internal carotid artery (ICA) elongations and wide carotid bulbs, but there was no evidence of stenosis or atherosclerosis. Intracranially a left longsegmented high-grade stenosis of the proximal M1-MCA segment could be conﬁ rmed. Distal to the stenosis, the residual M1 segment was mildly dilated. Also, a delayed contrast ﬁ lling of the distal MCA segments in relation to the distal anterior cerebral artery (ACA) segments was seen indicating a high-grade stenosis of hemodynamic relevance. There were no signs of vasculitis (Fig. B24.1 and Fig. B24.2).

Suspected Diagnosis

Asymptomatic left high-grade M1-MCA stenosis. In the absence of atherosclerotic vessel changes, and the presence of a history of left-sided facial pain with associated conjunctival injection and headache 1 year previously, an MCA dissection was suspected.

the day following it. The neurologic examination was normal; in particular, she did not have Horner’s syndrome.

MRI and MR Angiography (10:00 Hours)

No parenchymal lesions were seen on MRI. On T2-weighted axial MRI images, a distinctly reduced ﬂ ow void could be seen in the distal ICA on axial and coronal images. 3D time-of-ﬂ ight MR angiography (TOF-MRA) of the ce- rebral arterial circle (circle of Willis, CW) demonstrated the known left high-grade M1-MCA stenosis. A reduced signal was observed within the right terminal ICA. Cervical MRI and MRA of the extracranial vessels were not performed (Fig. B24.3 and Fig. B24.4).

Questions to Answer by Ultrasound Techniques

• To conﬁ rm the left-sided MCA stenosis.

• To assess collateral pathways if the stenosis was hemo-

dynamically relevant.

• To search for evidence of other vascular pathology, e.g.,

dissection of the right ICA.

Neurosonologic Findings (12:00 Hours)

Extracranial Duplex Sonography

There were no atherosclerotic vascular changes. The right ICA revealed a long-segmented lumen reduction that started 2 cm above the carotid bifurcation and continued over the whole visible distal vessel segment. There were no typical signs of a dissection. Flow velocity in the right ICA reached a systolic maximum of 200 cm/s. The right common carotid artery (CCA) showed a high-resistance ﬂ ow signal with a reduced diastolic ﬂ ow component. The left ICA, both external carotid arteries (ECAs), and the vertebral arteries (VAs) presented normal ﬂ ow signals (all images not shown).

Clinical Course (1)

Two wee ks lat er, th e pa ti en t wa s re ad mi tt ed t o o ur h os pital for further evaluation. On admission she reported a continuing right-sided neck pain that started during the catheter angiography 2 weeks before and a sore throat on

Transcranial Duplex Sonography

Within the left M1-MCA, transcranial color-coded sonography (TCCS) detected a turbulent stenotic ﬂ ow (ﬂ ow velocity 383/267 cm/s). A poststenotic ﬂ ow pat- tern was observed in the left M2-MCA branches. The ﬂ ow signal of the right M1-MCA segment appeared

381Conventional Angiography (16:00 Hours)

Fig. B24.1 (A) DSA, left ICA injection, left anterior oblique (LAO) projection. Mild elongation of the ICA and wide carotid bulb without evidence of atherosclerosis. (B) DSA, right ICA injection, right anterior oblique (RAO) projection. Identical mild elongation of the ICA and wide carotid bulb without evidence of atherosclerosis.

Fig. B24.2 (A) DSA, left ICA injection, posteroanterior view. Long high-grade stenosis of the proximal left M1-MCA (arrow). Note the dilation of the MCA distal of the stenosis. Also note the delayed ﬁ lling of the distal MCA segments in comparison to distal ACA segments. (B) DSA, left ICA injection, posteroanterior view. Magniﬁ ed view of A demonstrating a ﬁ liform MCA stenosis considered as dissection (arrows) and poststenotic vessel dilation

Fig. B24.3 (A) MRI T2-weighted image, axial plane, magnified view. Note the prominent right PCoA already visible (arrow). (B) MR T2-weighted image, axial plane, magnified view. Attenuated flow void in the right ICA (arrowhead) indicating a significantly reduced blood flow. Note the normal signal voids in the opposite ICA and BA.

normal. The right A1-ACA segment showed reversed ﬂ ow while the left-sided A1-ACA segment demonstrated increased ﬂ ow velocities without turbulence (ﬂ ow velocity 225/140 cm/s). Assessment of the posterior cerebral arteries, VAs, the basilar artery (BA), and the ophthalmic arteries (OAs) revealed overall normal antegrade ﬂ ow signals without signs of leptomeningeal or ophthalmic collateral support. There was a positive

Fig. B24.4 3D TOF-MRA, axial maximal intensity projection (MIP). Reduced signal in the left M1-MCA (single arrow), indicating highgrade stenosis. Note that the right-sided distinct PCoA seen in T2-weighted images is not visualized. Note also a reduced signal in the intracranial right ICA indicating severely compromised ICA ﬂ ow (arrows).

Conclusion

Hemodynamically relevant left high-grade M1-MCA s t e n o s i s . H i g h - g r a d e s t e n o s i s o f t h e r i g h t e x t r a c r a n i a l ICA of hemodynamic relevance, suspicious for dissection, induced by the diagnostic DSA 2 weeks previously. Excellent collateral ﬂ ow to the right MCA and ACA via the ACoA as well as the right PCoA.

oscillation eﬀ ect in the right M1-MCA segment with slight submandibular tapping of the left ICA and the dominant left VA at the atlas loop. This indicated collateral ﬂ ow through the anterior communicating ar- tery (ACoA) and right posterior communicating artery (PCoA) (Fig. B24.5, Fig. B24.6, Fig. B24.7, Fig. B24.8,

; see also Videos B24.1 and B24.2).

B24.9

Conventional Angiography (16:00 Hours)

DSA performed on the same day demonstrated a conical lumen reduction of the right ICA directly above the carotid bifurcation with a ﬁ liform stenosis up to the base of the skull which was suggestive of ICA dissection.

382 Case 24 Dissection of the Right Extracranial Internal Carotid Artery and Left M1 Middle Cerebral Artery

M1-MCA-L

Fig. B24.5 TCC S, tra nstempo ral ap proa ch, midbrai n plan e. Increased ﬂ ow velocity in the left M1-MCA indicating high-grade s t e n o s i s ( ﬂ ow velocity 383/267 cm/s).

A1-ACA-L

M1-MCA-R

Fig. B24.6 TCCS, tra nstem pora l app roac h, mi dbra in pl ane. Normal

ﬂ ow pattern in the right M1-MCA (ﬂ ow velocity 92/41 cm/s) despite the proximal extracranial high-grade ICA stenosis.

A1-ACA-R

Fig. B24.7 TCCS, transte mporal a pproach , midbra in pla ne, left sided insonation. Increased ﬂ ow velocity in the left A1-ACA without turbulence, suggesting collateralization of the contralateral anterior circulation via the ACoA but also for the ipsilateral MCA territory (ﬂ ow velocity 225/140 cm/s).

ACoA

Fig. B24.9 TCC S, t rans temp oral app roac h, mid brai n plan e, l eft sided insonation. Turbulent ﬂ ow and increased ﬂ ow velocity within the ACoA (functional stenosis) caused by intracranial cross-ﬂ ow from the left ICA. Note also the prominent blue-coded right PCoA (arrow).

Fig. B24.8 TCCS , transt emporal approac h, mid brai n plan e, righ tsided insonation. The right A1-ACA presented with reversed ﬂ ow direction (ﬂ ow velocity 83/30 cm/s). Note the eﬀ ect of contralateral ICA tapping on the ﬂ ow signal of the right A1-ACA assuring the cross-ﬂ ow via ACoA.

C o l l a t e r a l i z a t i o n t o w a r d t h e r i g h t M C A a n d A C A t e r r i t o r y was via the left ICA and ACoA. Selective VA angiography showed that the right MCA was also perfused by the ipsilateral PCoA. There was no evidence of ophthalmic collaterals. The known high-grade M1-MCA stenosis remained unchanged (Fig. B24.10, Fig. B24.11, Fig. B24.12). In addi- tion, renal angiography was performed, which excluded signs of ﬁ bromuscular dysplasia.

Clinical Course (2)

The dissection of the right ICA was considered to be of iatrogenic origin caused by the catheter during the initial DSA. Intravenous heparin treatment was started, aiming for a twofold rise in partial thromboplastin time (PTT). The patient was then switched to oral anticoagulation with phenprocoumon for 6 months. The etiology of the left M1-MCA stenosis remained

383Follow-up Neurosonologic Findings (6 Months)

Fig. B24.10 DSA, right ICA injection, RAO view. Conical lumen narrowing of the right ICA directly above the carotid bifurcation with a long-segmented ﬁ liform stenosis up to the base of the skull ( a r r o w s ) .

Fig. B24.11 DSA, left ICA injection, posteroanterior view. C o l l a t e r a l b l o o d ﬂ ow into the right MCA and ACA via ACoA and retrograde right A1-ACA. Symmetric ﬁ lling of both MCAs without delay between the right and left sides indicating well-developed cross-ﬂ ow (arrowheads). Also note the known long-segmental left M1-MCA stenosis (arrow).

Questions to Answer by Ultrasound Techniques

• Was there any regression of the right extracranial ICA stenosis under continuous anticoagulation with phenprocoumon?

• Were there changes in the left M1-MCA stenosis?

Follow-up Neurosonologic Findings (6 Months)

Extracranial Duplex Sonography

No ﬂ ow signal was observed in the right proximal ICA. The ipsilateral CCA revealed an increased pulsatility. The right ECA was normal revealing no indirect signs of collateral support (Fig. B24.13, Fig. B24.14, Fig. B24.15, B24.16). The left-sided carotid arteries and the VAs were unremarkable.

Fig. B24.12 DSA, left VA injection, posteroanterior view. C o l l a t e r a l b l o o d ﬂ ow via the marked PCoA (arrow) and distal ICA into the right MCA.

u n c l e a r . A f t e r e x c l u s i o n o f a l l o t h e r d i ﬀ erential d i a g n o s e s , p a r t i c u l a r l y v a s c u l i t i s , a d i s s e c t i o n w a s a s sumed to be most likely. After 6 months the patient was re-examined to evaluate the requirement for long-term secondary stroke prevention.

Transcranial Duplex Sonography

Intracranially the ﬂ ow pattern was unchanged in relation to the examination 6 months previously.

Conclusion

Unchanged high-grade stenosis of the left MCA. Secondary occlusion of the right extracranial proximal ICA with unchanged good collateral blood ﬂ ow via the ACoA and ipsilateral PCoA considered to be caused by dissection.

384 Case 24 Dissection of the Right Extracranial Internal Carotid Artery and Left M1 Middle Cerebral Artery

Conventional Angiography

Because of the unusual case history and assumed iatrogenic cause of the right-sided dissection the neuroradiologists recommended a further DSA which conﬁ rmed the occlu- sion of the right ICA with a smooth margin (Fig. B24.17).

Fig. B24.18 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries.

Clinical Course (3)

Secondary stroke prevention was changed to antiplatelet therapy. During 4 years of follow-up no cerebral ischemia occurred and no changes in vascular pathology were o b s e r v e d .

Final Diagnosis

Asymptomatic high-grade left M1-MCA stenosis presumably caused by spontaneous dissection. Iatrogenic dis-

CCA-L

section of the right extracranial ICA caused by catheter angiography with initial high-grade stenosis and secondary occlusion.

Discussion

Clinical Aspects

Here we report on a 34-year-old woman with a suspected left intracranial MCA dissection and an iatrogenic dissection of the right ICA.

Dissections are an important cause of stroke, especially in young patients. Most dissections, however, occur within the extracranial brain-supplying arteries. In these cases, diagnosis is mainly made by MRI visualization of the intramural hematoma. Other supporting indicators are the typical angiographic morphology, missing atherosclerotic vessel wall changes, and the presence of an intima ﬂ ap or a false lumen, in combination with a corresponding clinical picture (for further discussion on extracranial dissection, see Case 11 and Case 18).

CCA-R

Fig. B24.13 Extracranial duplex, longitudinal plane. Normal ﬂ ow in the left CCA (ﬂ ow velocity 122/49 cm/s, PI = 1.16).

ICA-L

Fig. B24.15 Extracranial duplex, longitudinal plane. Normal ﬂ ow in the left ICA (ﬂ ow velocity 65/30 cm/s).

Fig. B24.14 Extracranial duplex, longitudinal plane. High-resistance ﬂ ow signal in the right CCA demonstrating increased pulsatil- ity, i.e., a reduced diastolic ﬂ ow component (ﬂ ow velocity 127/22 cm/s, PI = 2.37).

ICA-R

Fig. B24.16 Extracranial duplex, longitudinal plane. Absent ﬂ ow signal in the right ICA.

ABC

Fig. B24.17 Follow-up DSA, right ICA injection, RAO views. (A) Initial DSA: Normal right ICA. (B) Two weeks later: High-grade ICA stenosis due to dissection. (C) After 6 months: Complete ICA occlusion with a rounded margin resembling occlusion in atherosclerosis.

385Discussion

Fig. B24.18 Schematic of the patient’s extra- and intracranial brain-supplying arteries. Right proximal ICA occlusion (large circle). Left M1-MCA stenosis (small circle). Collateral ﬂ ow of the right MCA territory from the left ICA via ACoA and retrograde A1-ACA as well as from the posterior cerebral artery (PCA) via the right PCoA. Collateralization of the left MCA territory via leptomeningeal collaterals from the left ACA.

Diagnosis of intracranial dissections is more diﬃ cult.

Often it is based on an angiographically diagnosed intracranial stenosis in a young patient suﬀ ering from a stroke accompanied by pain. In cases of a concomitant intracranial aneurysm or recent subarachnoid hemorrhage (SAH) the diagnosis becomes even more likely. However, in the group of patients aged >40 a reliable diagnosis becomes more diﬃ cult as atherosclerosis might be seen as a confounding factor and as headaches might also occur in “normal”-type stroke. In a meta-analysis of isolated MCA dissections, covering 54 selected publications and 61 cases, most of the patients included were of Asian ethnicity (62.3%) and of male gender (Asaithambi et al 2014). Ischemic stroke occurred in 79% and intracranial hemorrhage (ICH) in 69%—surprisingly high (for further discussion on intracranial dissection, see also Case 21).

In our case a MCA dissection was considered to be the most likely cause. In favor of this hypothesis were the reported left-sided facial pain and headaches, the young age of the patient, and the absence of atherosclerotic vessel wall changes. The angiographic ﬁ nding of an irregular long-segmental stenosis was also compatible with the hypothesis. However, no ischemia occurred and the stenosis remained unchanged over the following years. The latter is somewhat unusual for a dissection, as complete vessel restitution is frequent. A small study of six patients with intracranial VA dissection reported complete normalization in four of them (Kitanaka et al 1994a).

During catheter angiography for etiological clariﬁ cation of the MCA stenosis our patient experienced an extracranial ICA dissection with initial high-grade ICA stenosis and subsequent ICA occlusion. Clinically this corresponded to neck pains which the patient had experienced during and shortly after the ﬁ rst angiography. Because of the temporal coincidence and the subsequent discovery of typical angiologic ICA alterations, an iatrogenic cause seemed obvious.

Although rarely reported, the question was raised whether our patient had a particular predisposition to develop a dissection during selective catheter angiography because of an existing spontaneous intracranial dissection. An inherited or acquired abnormality of the intimal or medial vessel layers or of the elastic connective tissue, as for instance in Marfan’s syndrome, Ehlers–Danlos syndrome, and pseudoxanthoma elasticum, could result in increased vessel wall vulnerability (Schievink 2001), possibly also inducible by mechanical manipulations. Brandt and coworkers (1998) reported ultrastructural collagen alterations and alterations of the extracellular matrix in skin specimens of patients with extracranial dissections, which then may lead to generalized arteriopathy, associated intracranial dissecting aneurysms, an aortic dilatation, and/or hyperdistensibility of arterial walls (Guillon et al 2000, Hausser et al 2004). However, none of these conditions were found in our patient, and she had no suggestive family history. Therefore, the assumption of a particular predisposition to vessel wall injuries in our patient remains speculative.

Due to recent advances in noninvasive vascular d i a g n o s t i c s o f t h e b r a i n - s u p p l y i n g a r t e r i e s , a n g i o g r a p h y has lost its importance. However, it has, without doubt, a place in special indications such as the diagnosis of vascular malformations, vasculitis, or in any case where endovascular treatment is a potential therapeutic option. However, its use has always been open to criticism because of the potential side eﬀ ects. Although the tech- niques are constantly being improved by the use of smaller catheters, hydrophilic guidewires, and digital imaging systems, angiography-related neurologic complications still occur. Complication rates are usually reported as incidents occurring within 24 hours postintervention (so our case would not have been included).

A prospective analysis of 2,899 angiographic interventions revealed a combined rate of transient and reversible

386 Case 24 Dissection of the Right Extracranial Internal Carotid Artery and Left M1 Middle Cerebral Artery

neurologic deﬁ cits of 1.3%. In 14 of these patients (0.5%), persisting neurologic deﬁ cits occurred (Willinsky et al 2003). In an older report including eight prospective studies the general neurologic complication rate was

4.1% and the rate of persisting neurologic deﬁ cits was 1% (Hankey et al 1990). Complication rates are inﬂ uenced by patient-related as well as procedure-related factors. A signiﬁ cantly higher complication rate has been observed in patients aged ≥55 years (1.8% versus 0.9%) (Willinsky et al 2003). Other authors, who have reported no neurologic complications in those <50 years or those <30 years of age, support this ﬁ nding (Dion et al 1987, Heiserman et al

1994). Other factors are the duration of the angiography, the number of vessels catheterized, the experience of the investigator, and the vascular pathology studied. Thus, a four-vessel angiography is not a routine procedure and vessel intubation has to be justiﬁ ed on the basis of the clinical question itself. If a patient with anterior circulation pathology had a dissection during ICA intubation, the neuroradiologist would be at risk of being sued for malpractice. Mani and Eisenberg (1978) reported an overall complication rate of 3.9% in a teaching hospital, compared with 0.9% in a nonteaching hospital. When patients with and without occlusive artery disease were compared, the complication rates in a teaching hospital were 4.3% and

1.2%, and in a nonteaching hospital they were 2.6% and

0.5%, respectively (Mani et al 1978). The above ﬁ nding corresponds well with the fact that the rate of complications is higher in stroke patients in general than in those with other vascular pathology. A meta-analysis comparing stroke patients and patients with intracranial malformations, aneurysms, or vasospasm found a complication rate of 3% in the former group and 0.8% in the latter (Cloft et al 1999).

In addition to manifest neurologic deﬁ cits, angiogra- phy may also cause asymptomatic injuries to the brain. Bendszus and coworkers (1999) analyzed 91 patients who underwent a total of 100 mostly diagnostic angiographies. MRI including diﬀ usion-weighted images before and after angiography revealed 42 postinterventional new lesions in 23 patients, mostly of embolic appearance. Fortunately, none of these patients demonstrated a clinically detectable neurologic deﬁ cit. Patients with vascular risk factors and known vasculopathy were at higher risk of developing lesions than those without vascular pathology (44% versus 13%). The lesion size was small in the majority of cases but seven of them exceeded 10 mm (Bendszus et al 1999). This study illustrates that angiography-related embolic events are frequent but are not suﬃ ciently reﬂ ected by the reported clinical compli- cation rates. Considering the distribution pattern of the observed cerebral lesions, a thromboembolic event originating from the catheter itself or from mechanically dislocated atherosclerotic plaque fragments seems to be the most likely mechanism.

Side eﬀ ects related to the contrast agents used and, as in our case, a dissection of the vessel under study, occur less frequently. A retrospective analysis of 2,437 diagnostic angiographies and 675 neurointerventional procedures reported 12 dissections (0.4%); 9 of these were in the VA, 1 in the CCA, and 2 in the ICA (Cloft et al

2000). Seven of these patients reported symptoms during

contrast injection. In the remaining ﬁ ve the dissection occurred during catheter manipulation. Except for one patient who developed a clinically silent territorial infarction, all others had a benign clinical course.

Because of the symptom onset during angiography in our patient the diagnosis of a carotid dissection was beyond doubt. Interestingly, the patient did not mention her symptoms at the time of investigation, which was ambulatory. It was therefore missed and only noted when she was readmitted for further diagnostics and ultrasound depicted the new vessel pathology. This clinical pattern indicates that several dissections, and also those of spontaneous nature, might occur silently, leaving a potentially high number of unreported cases.

Angiologic and Anatomic Aspects

The primary ultrasound analysis yielded a long-segmented ICA narrowing with local systolic ﬂ ow velocities of up to 200 cm/s but no typical direct signs of dissection. Classically, a more distal located conical-shaped stenosis or occlusion can be found. Even if the stenosis itself is not visible, a high-resistance ﬂ ow signal might indicate the relevant distal ﬂ ow obstruction. The latter constellation alone, however, is not suﬃ cient to diagnose dissection, as distal stenosis caused by ﬁ bromuscular dysplasia (FMD) or a distal vessel kinking might result in similar ﬁ ndings. If atherosclerotic vessel wall changes are completely absent, a dissection becomes more likely, however. Whenever the patient shows additional head or facial pain and/or has Horner’s syndrome, the presence of a dissection is practically evident.

On the contrary, normal ultrasound ﬁ ndings do not exclude a dissection as a distal vessel narrowing <70–80% will not result in relevant proximal blood ﬂ ow alter- ations and distal dissecting aneurysms might dominate the morphologic picture. However, in our experience, if patients are symptomatic, a distal hemodynamically relevant stenosis is a frequent ﬁ nding. In patients without ischemia, extracranial ultrasound examination is normal in ~29% of cases. In those with ischemia, normal ultrasound ﬁ ndings occur in only 5% (Baumgartner et al 2001). An analysis of purely hemodynamic ultrasound criteria in patients with cerebral ischemia caused by a dissection found a sensitivity, speciﬁ city, and positive and negative predictive values of 96%, 92%, 94%, and 97%, respectively (Benninger et al 2006). Hence, ultrasound is especially useful as a screening tool in patients with stroke. Further radiologic examination will be needed for conﬁ rmation of diagnosis in equivocal cases (for further discussion on ultrasound ﬁ ndings in extracranial ICA dissection, see also Case 11 and Case 18).

During oral anticoagulation, our patient developed a secondary ICA occlusion which, in contrast with the patient in Case 11, did not result in an additional intracranial hemodynamic compromise (for further discussion on secondary vessel occlusion, see also Case 11). DSA demonstrated the hemodynamic eﬀ ect of the MCA stenosis by a delayed MCA vessel ﬁ lling when compared with the ACA contrast ﬁ lling pattern. Similar to DSA, ultrasound is also able to reveal ﬂ ow alterations induced by hemodynam- ically relevant stenoses. The ultrasound correlate of the

387Discussion

delayed vessel ﬁ lling is the presence of a poststenotic ﬂ ow pattern, which was observed in an M2 branch in our patient. Whenever a poststenotic ﬂ ow pattern is detected, a stenosis of at least 70–80% can be assumed. However, detailed grading, such as in extracranial ICA stenosis, is currently not possible (for further discussion on grading of intracranial stenoses, see Chapter 5, “Stenoses” under “Intracranial Pathology”).

Another interesting hemodynamic aspect was revealed by DSA. On selective VA ﬁ lling, the PCoA on the side of the ICA occlusion only provided blood ﬂ ow into the MCA territory while selective ﬁ lling of the contralat- eral ICA revealed a blood ﬂ ow from the ACoA into the ACA and MCA. This “task sharing” may be observed whenever more than one collateral pathway exists. Collateral ﬂ ow to the A1-ACA segment on the occluded side is then mainly provided via the contralateral A1-ACA segment, while ﬂ ow into the MCA of the occluded side is mainly derived from the ipsilateral PCoA.

In our case, the positive MCA signal reaction on the occlusion side during tapping of the VA as well as the contralateral ICA demonstrated the patency of both, the ACoA and the PCoA collateral. In addition to the above, the A1ACA on the nonoccluded ICA side not only provides blood via the ACoA to the contralateral side but also directly via leptomeningeal anastomoses to the ipsilateral MCA territory to compensate for the hemodynamically relevant ipsilateral M1-MCA stenosis. This phenomenon probably explains the unusual high ﬂ ow velocities of 225/140 cm/s. Remarkably, the MCA proﬁ le on the side of the ICA occlu- sion was normal without signs of hemodynamic impairment, indicating balanced intracranial hemodynamics. DSA correspondingly showed simultaneous ﬁ lling of both MCAs. This constellation may help to explain the benign

clinical course without occurrence of embolic or hemodynamically related ischemia over many years.

Another remarkable point is the morphologic evolution of the extracranial ICA dissection as seen in the DSA (see Fig. B24.17). Initially, the cone-shaped stenosis and the “string” or “rat tail” sign (Fig. B24.17B) conﬁ rmed the diagnosis of a dissection. Six months later, DSA demonstrated a rounded stump (Fig. B24.17C). A rounded vessel end is commonly considered to be typical of atherosclerotic ICA occlusions but it may appear in residual stages of ICA dissections (Houser and Baker 1984). This implies that a rounded ICA occlusion cannot be considered as pathognomonic of atherosclerotic origin and a chronic state following dissection is a relevant diﬀ erential diagnosis.

Intracranial TOF-MRA revealed known limitations, such as exaggerating the extent of MCA vessel pathology. The presence of distal M2-MCA branches, however, argued in favor of stenosis and against an occlusion. The weak signal of the contralateral intracranial ICA suggested a reduced ﬂ ow, later attributed to the detected dissection. Looking for vessel signals on conventional MRI images may be helpful. As in the assessment of venous thrombosis, a missing signal void of arterial vessels might indicate ﬂ ow obstruction. In our case the distinct reduction of carotid ﬂ ow was easily seen in the axial T2-weighted image (see Fig. B24.3B) which seems most suitable for ﬂ ow void assessment and in addition is easily available in almost any cranial MRI. Also, the prominent right PCoA, not visualized in the TOF-MRA (see Fig. B24.4) was detected without any problem in the axial T2-weighted image (see Fig. B24.3A). We therefore recommend that ultrasound users should always use the information provided by the other angiologic techniques to improve interpretation of the study results.

388

Case 25

Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery

Clinical Presentation

A 31-year-old woman was admitted with a transient mild paresis of the left arm lasting for 6 hours. One year ago she had been admitted to a district general hospital with a left-sided brachiofacial hemiparesis which had completely resolved within 4 weeks. Cerebral MRI at that time showed multiple right-sided ischemic l e s i o n s w i t h i n t h e m i d d l e c e r e b r a l a r t e r y ( M C A ) t e r r i t o r y (Fig. B25.1). Transcranial duplex sonography at that time revealed a right proximal high-grade MCA stenosis which was then conﬁ rmed by digital subtraction angiography (DSA) (Fig. B25.2). She had multiple vascular risk factors including arterial hypertension, heavy smoking, hyperlipidemia, obesity, and use of an estrogen-containing contraceptive. A cardiac embolic source had not been detected and she was given clopidogrel for long-term stroke prevention.

Initial Neuroradiologic Findings

Cerebral MRI on the day of this admission revealed the known old ischemic lesions which were partly territorial MCA infarction and partly internal and external border zone infarctions (Fig. B25.3). There was no evidence of any new ischemic brain lesions. Secondary widening of the anterior horn of the right lateral ventricle was observed.

Suspected Diagnosis

Right hemispheric transient ischemic attack (TIA) of embolic or hemodynamic origin caused by high-grade stenosis of the right M1-MCA segment, which had been detected 1 year before.

Questions to Answer by Ultrasound Techniques

• What was the status of the extracranial brain-supplying arteries?

• What was the status of the right MCA stenosis?

• Were there any potential collateral pathways?

Initial Neurosonologic Findings (Day 2)

Extracranial Duplex Sonography

B-mode imaging did not reveal any atherosclerotic vascular changes. Doppler spectrum analysis showed normal and symmetric ﬂ ow signals with no diﬀ erence in the pul- satility of the extracranial internal carotid arteries (ICAs) (Fig. B25.4

and Fig. B25.5).

Transcranial Duplex Sonography

The distal ICA and the carotid siphon showed normal ﬂ ow signals on both sides. The left proximal M1-MCA segment revealed a mildly stenotic ﬂ ow signal (ﬂ ow velocity 181/83 cm/s). Normal signals were observed in the corresponding M2 branches. The complete right M1-MCA segment could well be visualized using the color mode in a low ﬂ ow pulse repetition frequency (PRF) setting. Doppler ﬂ ow analysis revealed markedly reduced velocities without turbulence but with a mild poststenotic ﬂ ow pattern throughout its entire length (ﬂ ow velocity 17/10 cm/s). Doppler spectrum analysis of the left A1 anterior cerebral artery (ACA) segment was normal (ﬂ ow velocity 110/68 cm/s). The right A1- ACA segment revealed a mildly increased nonturbulent ﬂ ow (ﬂ ow velocity 156/84 cm/s). The ﬂ ow velocity in the right P2 posterior cerebral artery (PCA) segment was also increased (ﬂ ow velocity 105/57 cm/s) when compared with the left side (ﬂ ow velocity 61/25 cm/s). Also, a right-sided fetal-type PCA was seen (Figs. B25.6–

B25.11; see also Videos

B25.1 and B25.2).

Conclusion

Near-occlusion of the right M1-MCA with leptomeningeal collaterals from the ipsilateral ACA and PCA and mild M1-MCA stenosis on the left side.

Conventional Angiography (Day 4)

DSA was performed to clarify the suspected intracranial p a t h o l o g y . S i g n i ﬁ cant progression was found in comparison with the DSA performed 14 months previously. The nearocclusion of the right M1-MCA segment was conﬁ rmed and leptomeningeal collateralization was seen via the right ACA and PCA. No deﬁ nite caliber variations were described in the

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