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Case 11

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.

Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

269

Clinical Presentation

A 43-year-old man complained of transient right-sided weakness, amnesic aphasia, and decreased visual acuity in his left eye that started while he was undertaking exercise in a gym. The symptoms gradually faded over 15 minutes. The patient had no vascular risk factors except for a known migraine with aura. On admission to our hospital he was free of symptoms. Headaches were not reported. The neurologic examination revealed a mild left-sided Horner’s syndrome. There were no other focal neurologic deﬁ cits.

Initial Neuroradiologic Findings

Cerebral MRI on the day of admission showed no ischemic parenchymal lesion but perfusion imaging revealed a pronounced hypoperfusion within the left middle cerebral artery (MCA) territory and both anterior cerebral artery (ACA) territories. Time-of-ﬂ ight MR angiography ( T O F - M R A ) s h o w e d r e d u c e d s i g n a l i n t e n s i t y i n t h e l e f t distal internal carotid artery (ICA), left MCA, and both ACAs, as well as an aplasia or severer hypoplasia of the right A1-ACA segment and both posterior communicating arteries (PCoAs) (Fig. B11.1 and Fig. B11.2). The cervical vessels were not examined, yet axial T2-weighted images at the level of the skull base suggested an intramural hematoma of the left ICA.

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode ultrasound did not show atherosclerosis or other structural vessel abnormalities and no direct signs of vessel dissection. Color-mode imaging of the left ICA demonstrated a tapering lumen and reduced color signal intensity. Doppler spectrum analysis revealed a pronounced reduction of ﬂ ow velocity (28/8 cm/s) in contrast with the contralateral side (78/26 cm/s) (Fig. B11.3 and Fig. B11.4; see also Video artery (ECA) had an increased diastolic, i.e., an “internalized,” blood ﬂ ow pattern. Assessment of the vertebral ar- teries (VAs) was normal.

Transcranial Duplex Sonography

A poststenotic ﬂ ow pattern was observed in the left carot- id siphon, the left M1-MCA segment, and the left A1-ACA segment. No right A1-ACA segment and no ﬂ ow signal in the presumed area of both PCoAs were detected. The ﬂ ow direction in the left OA was reversed and showed a high diastolic ﬂ ow component similar to that of a brain-sup- plying artery. The right OA was normal. Assessment of the posterior circulation was unremarkable and without evidence of collateral leptomeningeal ﬂ ow (Figs. B11.5– B11.10; see also Videos

B11.1). The external carotid

B11.2 and B11.3).

Suspected Diagnosis

Dissection of the left ICA.

Suspected dissection of the left ICA with high-grade stenosis of hemodynamic relevance below the OA origin. Insuﬃ cient intracranial collateral blood ﬂ ow toward the left MCA and both ACA territories solely via the left OA.

Questions to Answer by Ultrasound

Conclusion

Techniques

• Was there evidence of dissection, high-grade stenosis, or occlusion of the ICA?

• If so, was there evidence of collateral blood ﬂ ow via the ACA, PCoA, ophthalmic artery (OA), or leptomeningeal vessels via the posterior cerebral artery (PCA)?

Clinical Course (1)

Intravenous heparin was started, aiming for a doubling of partial thromboplastin time (PTT). During the patient’s ﬁ rst night in hospital, he developed a severe right-sided brachiofacial paresis and a global aphasia. Laboratory monitoring revealed a fourfold increase in PTT. Intracranial bleeding was ruled out by a CT scan.

270 Case 11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

Questions to Answer by Ultrasound Techniques

• Was the clinical worsening caused by a thromboembolic event with secondary occlusion of distal MCA branches or by hemodynamic impairment due to stenosis progression or occlusion of the ICA?

• If an occlusion of the ICA was present, which collateral pathways were activated in comparison with the initial investigation?

Follow-up Neurosonologic Findings (Day 2)

Extracranial Duplex Sonography

B-mode imaging of the left ICA remained unchanged. However, Doppler spectrum analysis now demonstrated a high-resistance ﬂ ow signal with a low and short systol- ic ﬂ ow and completely absent diastolic ﬂ ow component indicating distal ICA occlusion proximal to the OA origin (Fig. B11.11).

Transcranial Duplex Sonography

A worsened poststenotic ﬂ ow pattern was observed in the left M1-MCA and A1-ACA segments. Furthermore, there was an increase of retrograde ﬂ ow in the left OA. Raised ﬂ ow velocity in the left P2/3-PCA segments, pre- viously not observed, indicated leptomeningeal collateral ﬂ ow from the PCA to the left anterior territory (Fig. B11.12, Fig. B11.13, Fig. B11.14, Fig. B11.15).

Conclusion

Secondary distal occlusion of the left ICA. Further worsening of the pre-existing insuﬃ cient blood ﬂ ow in the left MCA and both ACA territories. Collateralization via the left OA and in addition via leptomeningeal collaterals from the left PCA.

Fig. B11.16 shows a schematic drawing of the extra-

and intracranial brain-supplying arteries.

Clinical Course (2)

CT angiography (CTA) demonstrated a left intracranial ICA occlusion in its petrosal part. The beginning of the dissection was assumed to be located in the midcervical extracranial ICA (Fig. B11.17). None of the studied intraand extracranial arteries showed evidence of ﬁ bromuscu- lar dysplasia. Under hypervolemic treatment the aphasia and the hemiparesis improved slowly over subsequent days. Six days after admission, cerebral MRI revealed a large internal border zone infarction (BZI) between the left ACA and MCA territories (Fig. B11.18).

Follow-up Neurosonologic Findings (Day 7)

Extracranial Duplex Sonography

Partial reopening of the left ICA was seen, now demonstrating a ﬂ ow signal similar to that on day 1 (Fig. B11.19; see also Video

B11.4).

Transcranial Duplex Sonography

A continuing poststenotic ﬂ ow pattern was seen within the left M1-MCA and A1-ACA segments. However, ﬂ ow velocities had slightly increased. The OA ﬂ ow was still re- versed indicating a persisting hemodynamically relevant ICA obstruction below the origin of the OA (Fig. B11.20; see also Video

B11.5 and B11.6).

Conclusion

Partial reopening of the distal ICA with a remaining hemodynamically relevant high-grade stenosis. The result is equivalent to the neurosonologic ﬁ ndings on admission.

Clinical Course (3)

Tre atm ent was cha nge d fr om h epa ri n to con tin uous ora l anticoagulation with phenprocoumon. Three weeks after admission the patient was clinically stable and was discharged with a moderate right-sided paresis and motor aphasia.

Follow-up Neurosonologic Findings (6 Months)

Extracranial Duplex Sonography

The left ICA had normalized (Fig. B11.21; see also Video

Transcranial Duplex Sonography

The left MCA and ACA as well as the PCAs demonstrated normalized ﬂ ow velocities and pulsatility. The ﬂ ow direc- tion of the left OA was now antegrade (Fig. B11.22, Fig.

B11.23, Fig. B11.24, Fig. B11.25; see also Video

Conclusion

Flow normalization in the left ICA without signs of intracranial collateral blood ﬂ ow, indicating hemodynamic normalization.

B11.7).

B11.8).

271Final Diagnosis

Final Diagnosis

Spontaneous dissection of the left ICA in a patient with unfavorable cerebral arterial circle (circle of Willis) due

Fig. B11.1 (A) MRI, apparent diﬀ usion coeﬃ cient (ADC) map, axial plane. No signs of cytotoxic edema. (B) MR T2* perfusion image (time-to-peak map), axial plane. Pronounced hypoperfusion indicated by a brighter signal within the left MCA and both ACA territories.

to a nonfunctional right A1-ACA and nonfunctional bilateral PCoAs. Secondary transient occlusion, presumably triggered by anticoagulation with intravenous heparin, leading to internal BZI.

Fig. B11.2 3D TOF-MRA, axial maximal intensity projection (MIP). Reduced signal intensity in the left intracranial ICA (arrows), left MCA (large arrowhead), and ACA (small arrowhead) indicating reduced ﬂ ow in these vessels. Note the missing signals in the right A1-ACA (arrow) and the PCoAs, suggesting aplasia or severe hypoplasia.

ICA-L

Fig. B11.3 Extracranial duplex, longitudinal plane. Tapering vessel size and pronounced reduction of blood ﬂ ow in the left ICA distal of the bifurcation (ﬂ ow velocity 28/8 cm/s).

ICA-R

Fig. B11.4 Extracranial duplex, longitudinal plane. Right ICA with normal ﬂ ow signal (ﬂ ow velocity 78/26 cm/s).

272 Case 11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

M1-MCA-L

Fig. B11.5 TCCS (trans temporal appro ach) , lef t-si ded i nson ation midbrain/thalamic plane. Poststenotic ﬂ ow pattern in the left M1- MCA (ﬂ ow velocity 31/20 cm/s).

M1-MCA-R

A1-ACA-L

Fig. B11.6 TCCS (tran stemporal appro ach) , left -sid ed ins onati on, midbrain plane. Poststenotic ﬂ ow pattern in the left A1-ACA (ﬂ ow velocity 32/20 cm/s). Note that the correct PI is 0.5.

OA-L

Fig. B11.7 TCC S (trans temp oral a ppro ach), righ t-sided in sonation midbrain plane. Normal ﬂ ow in the right M1-MCA (ﬂ ow velocity 94/46 cm/s).

OA-R

Fig. B11.9 TCCS (tra nsor bita l ap proa ch), r ight- side d in sonatio n. Normal ﬂ ow direction in the right OA (ﬂ ow velocity 65/20 cm/s).

Fig. B11.8 TCCS (tr anso rbital appr oach ), l eft- sided inson atio n. Re versed ﬂ ow direction and increased ﬂ ow velocity in the left OA (ﬂ ow velocity 70/40 cm/s).

P2-PCA-L

Fig. B11.10 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , thalamic plane. Normal ﬂ ow velocity in the distal left P2-PCA (ﬂ ow velocity 46/28 cm/s).

273Final Diagnosis

ICA-L

Fig. B11.11 Extracranial duplex, longitudinal plane. High-resistance ﬂ ow signal with a low and short systolic ﬂ ow and completely absent diastolic ﬂ ow component considered to correspond to distal left ICA occlusion proximal to the OA origin.

A1-ACA-L

M1-MCA-L

Fig. B11.12 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Further worsening of the pre-existing marked compromised poststenotic ﬂ ow pattern in the left M1-MCA (ﬂ ow veloc- ity 25/14 cm/s). Note the positive oscillation eﬀ ect caused by slight digital tapping of the left optic bulb (arrows).

P2-PCA-L

Fig. B11.13 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Similar worsened poststenotic ﬂ ow pattern in the left A1-ACA (ﬂ ow velocity 25/10 cm/s).

OA-L

Fig. B11.15 TCCS ( tran sorbital a pproach ), lef t-si ded in sona tion. Further increase of the rever sed ﬂ ow in the left OA (ﬂ ow velocity 97/54 cm/s).

Fig. B11.14 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain/thalamic plane. Increased ﬂ ow velocity in the left distal P2-PCA indicating leptomeningeal collateral ﬂ ow (ﬂ ow velocity 122/53 cm/s).

274 Case 11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

Fig. B11.16 Schematic of this patient’s extra- and intracranial brain-supplying arteries. Note the left distal ICA occlusion (circle). Collateral blood ﬂ ow is via the left ECA and retrograde OA toward the left MCA and ACA as well as to the right ACA territory. There is additional leptomeningeal collateralization of the left MCA territory after secondary occlusion via the left PCA (green arrow).

Fig. B11.17 CTA, curviplanar sagittal ICA reconstruction. Occlusion of the left ICA in its petrosal part (arrowhead). Note the beginning of the dissection in the middle segment of the extracranial ICA (arrows).

Fig. B11.18 MR FLAIR-weighted image, axial plane. Large internal BZI between the left ACA and MCA territories.

ICA-L

Fig. B11.19 Extracranial duplex, longitudinal plane. Partial reopening with low ﬂ ow signal in the left ICA similar to the ﬁ ndings on admission (ﬂ ow velocity 30/20 cm/s).

275Final Diagnosis

M1-MCA-L

Fig. B11.20 TCC S (t ranstem pora l ap proach) , left-s ided ins onation, midbrain plane. Ameliorated poststenotic ﬂ ow pattern with increase of ﬂ ow velocity in the left M1-MCA (ﬂ ow velocity 44/30 cm/s), similar to the ﬁ ndings of the ﬁ rst examination.

M1-MCA-L

ICA-L

Fig. B11.21 Extracranial duplex, longitudinal plane. Further normalization of the left ICA ﬂ ow (ﬂ ow velocity 47/24 cm/s).

A1-ACA-L

Fig. B11.22 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 88/43 cm/s).

OA-L

Fig. B11.24 TCCS ( tran sorbital a pproach ), lef t-si ded in sona tion. Normalized antegrade ﬂ ow in the left OA (ﬂ ow velocity 45/12 cm/s).

Fig. B11.23 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , midbrain plane. Normalized ﬂ ow signal in the left A1-ACA (ﬂ ow ve- locity 110/47 cm/s). Note the distinct ﬂ ow velocity compared with the left M1-MCA, indicating blood supply to both A2-ACAs.

P2-PCA-L

Fig. B11.25 TCCS (trans temp oral ap proa ch), lef t-sid ed i nson ation , thalamic plane. Normalized ﬂ ow signal in the left distal P2-PCA (ﬂ ow velocity 51/27 cm/s).

276 Case 11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

Discussion

Clinical Aspects

Cervical arterial dissections (CADs) of the brain-supplying arteries are usually thought to be caused by an intimal tear, which allows blood to enter between the layers of the arterial wall resulting in intramural hematoma. Alternatively, bleeding of the vasa vasorum is thought to be the cause of the intramural hematoma if no tear is present. Most frequently the hematoma is found within the medial layer. From there it may evolve toward the subintimal or subadventitial compartments. A dissection with accumulation of blood between the intima and the media is more likely to cause vessel stenosis or occlusion. A dissection path between the media and the adventitia may lead to the development of aneurysms.

Dissections can be divided into spontaneous and traumatic (Mokri 1990). The pathogenesis of a spontaneous dissection is unknown but increased vessel wall vulnerability seems likely, especially as there is a link to known connective tissue disorders such as Ehlers–Danlos and Marfan’s syndromes and ﬁ bromuscular dysplasia. Mild ultrastructural connective tissue alterations have been found in 68% of patients with spontaneous dissection despite the absence of any skin, joint, or skeletal abnormalities (Brandt et al 1998, Brandt et al 2001). Furthermore, in spontaneous CAD it has been assumed—based on analysis of the superﬁ cial temporal artery—that leakage of neoangi- ogenetic capillaries, which branch from the vasa vasorum, leads to the formation of microhematomas along the medial/adventitial border and to a disintegration of the vessel texture. Rupture of these capillaries and the vasa vasorum might be the consequence, with bleeding into the medial layer or the border zone between the medial and adventitial layer leaving the intima intact (Völker et al 2011). Familial occurrence and heritable connective tissue disorders in CAD seem rare. In a study of 1,934 consecutive patients, this was found in only 20 (1%) cases, predominantly aﬀ ecting the ICA (Debette et al 2014). Arterial tortuosity, such as kinking and coiling, seemed also to increase vessel vulnerability and has been related to ICA dissections (Saba et al 2015). The potential link with common vascular risk factors such as smoking, hypertension, or oral contraceptives has not yet been evaluated in larger studies. Atherosclerosis appears to be distinctly uncommon in these patients. The predominance in autumn and winter indicates a relationship to recent infections (Kloss et al 2012).

ICA-CAD usually starts 2–3 cm above the carotid bifurcation, extending distally over a variable length. A continuation of the dissection into the intracranial but extradural vertical part of the C6 segment of the ICA is unusual (de Bray et al 2007, Schievink 2001). Dissection of the intracranial intradural ICA segments is rare (Huang et al 2007). In most cases only a single artery is aﬀ ected, but multi- ple CAD may occur in up to 15%. The latter was shown to be more frequent in patients with preceding trauma or cervical manipulation (Béjot et al 2014). However, another recent study comparing spontaneous with traumatic carotid and vertebral artery dissections revealed similar percentages of single and multiple dissections (Lleva et al

2012). Multiple CAD makes an underlying connective tis-

sue disease more likely (Schievink et al 1994a). In the case presented here, the medical history is free of connective tissue diseases and no signs of ﬁ bromuscular dysplasia were seen by conventional angiography.

Like spontaneous CADs, traumatic dissections also originate predominantly from the most mobile segments of an artery (Lleva et al 2012). The V3-VA segment, the border between the V1 and V2-VA segments, and the distal extracranial ICA at the level of the ﬁ rst and second cervical vertebrae are therefore particularly vulnerable regions. In patients with extensive dissections involving almost the entire extracranial part of both ICAs and VAs, the point of origin is deﬁ ned by the most proximal part of the vessel pathology.

Spontaneous dissections of the carotid or vertebral arteries occur in only ~2% of all ischemic strokes. However, they are an important cause of stroke in young and middle-aged patients (15–49 years) and may even be underdiagnosed in elderly patients (Ahl et al 2004). In the young, spontaneous dissections account for 15–25% of cases (Schievink and Roiter 2005, Putaala et al 2009). Extracranial arteries are more frequently aﬀ ected than intracranial vessels (for further information about intracranial dissections, see Case 21 and Case 24). The annual dissection rate in the extracranial ICA (3 per 100,000 per year) is twice as high as in the extracranial VA (1.5 per 100,000 per year) (Schievink and Roiter 2005) (for further discussion of VA dissections, see Case 19 and Case 26).

Patients with traumatic dissection always report an episode of head or neck injury (for further reading on traumatic dissection, see Case 18). The question of whether trivial trauma may contribute to a cervical dissection is still a matter of debate. There are reports of dissections in association with Valsalva maneuver, coughing, sneezing, vomiting, defecation, sexual activity, or chiropractic neck manipulation (Dziewas et al 2003, Engelter et al 2013, Reuter et al 2006). Furthermore, dissections have been reported during physical exercise such as volleyball or tennis, or even after sudden turns of the head (Luken et al 1979). It is thought that a sudden hyperextension or rotation of the neck may then injure the ICA or VA as a result of mechanical stretching (Hufnagel et al 1999, Schievink 2001). The Cervical Dissection and Ischemic Stroke Patients (CADISP) study reported that 40.5% of patients with dissection recalled prior trauma, 88% of which was mild (Engelter et al 2013). However, there are no reliable statistics to assess the actual risk of having a dissection due to abrupt movements of the cervical spine (Brandt and Grond-Ginsbach 2002).

Our patient reported that his symptoms started during mild exercise in a gym, but he denied any sudden hyperextension or rotation of the neck. However, he had a history of migraine with visual aura—a condition which has been associated with spontaneous cervical artery dissections and is considered to be an independent risk factor. In a hospital-based case–control study migraine was diagnosed in 49% of patients with spontaneous dissection (Tzourio et al 2002). Another case–control study including 72 patients found the incidence of migraine to be 60% compared with 30% in the control group of infarcts without a dissection and 18% in healthy controls (Pezzini et al 2005).

277Discussion

With regard to gender diﬀ erences, a study of 696 patients with dissection, the incidence of migraine in women was 47% compared with 20% in men (Arnold et al 2006b).

In spontaneous ICA dissection, pain is the most common clinical sign. It occurs in the form of headaches and facial or neck pain in ~60% of cases and during the course of the disease in ~75% of patients. As a sole manifestation, pain may appear in up to 4.5%. Unilateral pain is more frequent then bilateral pain and headache in ICA dissection may be confounded with a migraine attack. Interestingly, our patient with a known history of migraine did not experience dissection-related headaches.

Horner’s syndrome is considered to be a typical clinical feature of carotid dissection and was also present in our patient. Overall, it has only been observed in 40% of cases with ICA dissection. Isolated Horner’s syndrome may be seen in ~10% of cases. Cranial nerve palsies, mostly aﬀ ecting nerves IX–XII, are found in up to 16% of pa- tients (Baumgartner and Bogousslavsky 2005).

Cerebral or retinal ischemia occurs in ~75% of spontaneous ICA dissection. In an analysis of 145 symptomatic patients, Baumgartner found ischemic stroke to be the most common manifestation aﬀ ecting 80% of cases, fol- lowed by cerebral transient ischemic attack (TIA) in 15%. Amaurosis fugax was present in 1% of cases and a retinal infarct occurred in 5% of patients (Baumgartner et al

2001). Retinal TIAs, as in our patient with reduced vision, can be caused by embolism, such as in the typical amaurosis fugax, or may be of hemodynamic origin due to a diminished blood ﬂ ow toward the optic nerve. The inci- dence of a hemodynamically related visual impairment might be underestimated, as it does not cause a typical transient monocular blindness (Biousse et al 1998).

In the majority of cases neuroimaging reveals territorial MCA infarctions, suggesting arterial embolism as the main cause of stroke in ICA dissection. In a study of 130 patients with brain infarction after ICA dissection, only one patient had an ACA infarction; all others had territorial MCA infarcts. In 5% of patients, additional BZIs were observed. In this study, BZI alone did not occur (Benninger et al 2004). Other studies reported an incidence of BZI of up to 16% (Steinke et al 1996). In contrast, hemodynamic BZIs in patients with atherosclerotic symptomatic highgrade ICA stenoses or occlusions have been observed in ~50% of cases (Szabo et al 2001). This diﬀ erence may in part be explained by better and more eﬀ ective collateral pathways in the younger dissection population (for further discussion on BZI, see Chapter 4, “Border Zone Infarction” under “Arterial Ischemia,” and Case 30).

There is no evidence-based recommendation for the therapeutic management of cervical artery dissection in the acute and subacute phase and for long-term secondary prevention. Avoiding low arterial blood pressure is a well-accepted way to impede hemodynamic stress and a BZI in the acute phase. Currently initial PTT-guided anticoagulation with intravenous heparin is often the initial treatment, aiming to prevent secondary embolism, followed by oral anticoagulation for 3–6 months, but others advocate antiplatelet drugs. According to the published CADISS trial which enrolled 250 patients with dissection of the ICA and VA, oral anticoagulation, and antiplatelet therapy had no statistically relevant eﬀ ect

in the prevention of relapsing stroke or TIA. After exclusion of 52 patients who failed dissection conﬁ rmation in the central image review process, stroke occurred in 3 of 101 patients (3%) in the antiplatelet group and in 1 of 96 patients (1%) in the anticoagulant group (Markus et al 2015). There was no death in either group but one major bleeding in the anticoagulant group. Similar ﬁ nd- ings were reported in smaller studies (Kremer et al 2003). Antiplatelet therapy may be the ﬁ rst choice for patients who have no ischemic neurologic symptoms caused by intracranial dissection and in dissecting stenoses if no or nonfunctional communicating arteries are present. In the latter, anticoagulation may lead to secondary increase of the intramural hematoma, which might cause pain recurrence, progression of stenosis, or even secondary vessel occlusion. A study of 20 patients with ICA stenosis caused by dissection reported a delayed occlusion in 5 patients (25%) during heparin therapy. These patients had much higher PTT values than those without delayed occlusion, indicating the importance of careful PTT control (Dreier et al 2004). Our patient was the only one of this group who clinically deteriorated because of his particularly unfavorable collateral pathways. A similar rate of secondary vessel occlusion (29%) was also reported by Dittrich et al (2006).

We recommend tailoring treatment strategies according to the condition of the individual patient. As arterial embolism seems to be the greatest risk in the acute stage, initial PTT-guided heparin treatment should be attempted, at least if microembolic signals are detected during transcranial ultrasound. Assessment of the circle of Willis and the collateral function should be part of the initial examination. In cases without cerebral ischemia or impaired collaterals, aspirin and blood pressure stabilization may be preferred treatment options.

In artery-to-artery embolism caused by extracranial dissection systemic recombinant tissue plasminogen activator (rt-PA) thrombolysis in stroke is probably safe. In a small study of 11 thrombolyzed patients with ICA dissection there were no deaths, only one patient had a symptomatic hemorrhage, and four patients had an excellent outcome (Derex et al 2000). In a second report of 33 patients with ICA dissection no local worsening, such as the formation of aneurysms or vessel rupture, was observed. A modiﬁ ed Rankin scale (m-RS) <2 was seen in 52% of cases (Georgiadis et al 2005). On the base of these data, it seems reasonable to perform systemic thrombolysis within the usual time window in patients with signs of cerebral ischemia. A clear clinical beneﬁ t of systemic thrombolysis in selected stroke patients with spontaneous CAD has not yet been shown. However, none of the studies diﬀ erentiated between patients with and without distal vessel occlusion (Engelter et al 2012, Zinkstok et al

2011). Contrary to spontaneous dissections, intravenous thrombolysis is not recommended in traumatic CAD due to the increased risk of intracranial and systemic hemorrhage (Nedeltchev and Baumgartner 2005). For further reading on mechanical thrombectomy in cervical dissection, see Case 18; for further reading on mechanical thrombectomy in intracranial occlusion, see Case 10.

The recommended 3–6 month period of oral anticoagulation is partly based on follow-up ultrasound studies

278 Case 11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

showing recanalization within this timeframe in most cases. During the recanalization process, oral anticoagulation might prevent downstream arterial embolism, but this assumption is not evidence-based. After its discontinuation, secondary prophylaxis with platelet inhibitors is sometimes recommended on an empirical basis. This might be particularly useful in patients with concomitant atherosclerosis and if the dissection led to the formation of persistent extracranial aneurysm (see also Case 26).

Recanalization after ICA dissection, as in our patient, is a frequent ﬁ nding. In the case of an initial stenosis res- titution occurs in ~70%, most often completely. In vessel occlusions at least a partial recanalization will take place in ~90% of cases. The process can start immediately and may be completed within the ﬁ rst weeks (Steinke et al

1994). Continuing vessel restitution beyond a period of 3 months is unlikely. In rare cases, however, it may occur even after a year (Baracchini et al 2010). Restitution of the vessel lumen may be observed, partial in ~20–40% and complete in ~50–60%, but in around 10–20% the occlusion persists. Recanalization rates are similar in ICA and in VA dissection (Baracchini et al 2010, Bartels and Flügel 1996, Nedeltchev et al 2009). Dissecting aneurysms may be found in about up to half of the ICA dissections. They have been reported to persist in 46%, to disappear in 36%, and to decrease in size in 18% during observation over a period of several years. Aneurysm enlargement has not been described in the literature. The general prognosis is good and stenting or prolonged oral anticoagulation is not recommended (Guillon et al 1999, Touzé et al 2001).

The clinical long-term outcome is good, independent of recanalization or persistence of occlusion. The annual stroke rate for the ipsilateral carotid territory was found to be 0.3% in reopened vessels and 0.7% in permanently occluded vessels (Kremer et al 2003). The risk of a recurrent dissection in a patient without a family history or connective tissue disorder is low, at ~1% per year (Schievink and Roiter 2005). Recurrence seems also independent from the use of antiplatelet or anticoagulant treatment. In the CADISS trial, ipsilateral stroke recurrence was observed in only 4 of 250 patients (2%; Markus et al 2015).

Angiologic and Anatomic Aspects

Ultrasound near the carotid bifurcation yields information about the vessel lumen as well as mural and intramural structures. However, the most common sites of ICA dissection, in contrast with atherosclerotic lesions, are at the midcervical region of the ICA or near the base of the skull. The intramural hematoma usually starts further downstream and dissecting aneurysms may involve any segment along the aﬀ ected artery. There- fore, direct morphologic signs may not be detected with duplex ultrasound. A digital subtraction angiography (DSA) study in patients with ICA dissection demonstrated stenoses in 50% of cases, vessel occlusion in 30%, and vessel dilatation or dissecting aneur ysms in the remainder (Pelkonen et al 2003). Other authors using DSA, CTA, and MRA found occlusion rates of up to 51% (Dziewas et al 2003).

Duplex sonography is a well-established method

to evaluate 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 BFV measurements exist to diagnose CAD. Typical direct ultrasound ﬁ ndings are (1) irreg- ular stenosis with an eccentric narrowing channel, (2) thickened hypo- or isoechoic vessel wall resembling hematoma, (3) irregular vessel membrane with double lumen, (4) local vessel distension, and (5) a dissecting aneurysm (Alecu et al 2007, Bartels and Flügel 1996, Lu et al 2000, Touboul et al 1988) (for further reading see Chapter 5, “Dissection” under “Vessel Wall Pathology”). Indirect hemodynamic ﬁ ndings in CAD are the same as seen in high-grade arteriosclerotic stenosis or occlusion (for further reading on indirect hemodynamic ultrasound ﬁ ndings see also Chapter 5, “Collat- eral Pathways,” and Case 15). The sensitivity of duplex sonography is remarkably lower if only direct signs are taken into consideration and has been reported to be 43% (Alecu et al 2007).

When performing duplex sonography in high-grade dissecting stenosis, care should be taken in cases with long-segment stenosis and near-occlusions as intrastenotic ﬂ ow velocity might be normal or even reduced. Fur- thermore, embolic occlusions of distal vessel segments may result in reduced ﬂ ow velocities in the extracranial ICA. However, none of the above ﬁ ndings are pathogno- monic for a dissection. Pre- and poststenotic vessel segments will show the familiar pre- and poststenotic ﬂ ow patterns on which, for example, the presumed diagnosis of a distal ICA dissection may be based. A systematic ultrasound analysis of hemodynamic parameters in 70 patients with known distal ICA dissection revealed the following ﬁ ndings: A right-to-left diﬀ erence in common carotid artery (CCA) resistance index of >10% in 85.7%, an >30% ipsilateral CCA ﬂ ow reduction in 78.6%, an ip- silateral biphasic ICA ﬂ ow indicative of distal occlusion in 45.7%, an increased distal ICA ﬂ ow velocity (deﬁ ned as an ipsilateral ICA/CCA and ipsilateral ICA/contralateral ICA systolic ﬂ ow velocity >1.5) in 8%, and a retrograde OA ﬂ ow in 38% of cases. Direct morphologic abnormal- ities, considered to be dissection speciﬁ c, were clearly less present with a tapering occlusion in 11.4%, a double lumen in 7.1%, and a localized ectasia distal of the carotid bulb with concomitant eccentric narrowing suggestive of intramural hematoma in 21.4% of cases. A hypoechoic or anechoic intraluminal formation alone was not considered to be a speciﬁ c ﬁ nding, as it could also correspond to a mural thrombus or an anechoic plaque. A concomitant enlargement of the vessel diameter is, however, a highly speciﬁ c sign of a dissected pathology. Combin- ing direct and indirect signs, a sensitivity of 90% and speciﬁ city of 60% were reported in an analysis of 70 patients with ICA dissections compared with MRI and conventional angiography (Alecu et al 2007). Another study including 181 patients with 200 spontaneous ICA dissections assessed the extracranial as well as intracranial hemodynamics. Pathologic extracranial/intracranial ultrasound results in 145 patients with and 55 patients without cerebral and/or retinal ischemia were present in 95% versus 30% and 71% versus 4%, respectively. An

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