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Case 19

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.

Bilateral Extracranial Vertebral Artery Dissection with Distal Occlusion of the Right Vertebral Artery

339

Clinical Presentation

A 29-year-old woman was admitted with symptoms of acute vertigo and unsteadiness, accompanied by nausea and vomiting. She had no vascular risk factors except that she had migraines and used an estrogen-containing contraceptive pill. Two weeks prior to admission she had had a mild respiratory tract infection.

On admission, the neurologic examination revealed spontaneous nystagmus in addition to a gaze-evoked nystagmus to the right side. Initially, a left-sided vestibular neuropathy was suspected. The day after admission she reported a new neck pain on the right side and occipital headaches of moderate intensity. Clinical examination revealed mild right limb ataxia and unsteadiness with drifting to the right side. The head thrust test was normal on both sides (National Institute of Health Stroke Scale [NIHSS] score: 2).

Initial Neuroradiologic Findings

Cerebral MRI showed a subacute cerebellar ischemic infarction in the right posterior inferior cerebellar artery (PICA) territory (Fig. B19.1). No sign of intramural hematoma was observed on axial T1-and T2-weighted images. Time-of-ﬂ ight MR angiography (TOF-MRA) re- vealed absence of right distal vertebral artery (VA) signals (Fig. B19.2). The left VA was normal. A fetal-type posterior cerebral artery (FT-PCA) was seen on the right side. The basilar artery (BA) and all other intracranial vessels were unremarkable.

Initial Neurosonologic Findings

Extracranial Duplex Sonography

Normal ﬂ ow signals were found in the carotid arteries. The left VA was inconspicuous with a constant diameter of 3.9 mm in the V1 and V2 segments. The diameter of the right V1-VA and proximal V2-VA was 3.0 mm. The distal perfused lumen of the right V2-VA was highly variable, ranging from 1.7 mm to 2.6 mm. Doppler spectrum analysis demonstrated a high-resistance ﬂ ow signal with a low and short systolic ﬂ ow and completely absent diastolic ﬂ ow component in its extracranial segments (Fig. B19.3, Fig. B19.4, Fig. B19.5, Fig. B19.6, Fig. B19.7; see also Video

B19.1).

Transcranial Duplex Sonography

Transtemporal insonation revealed normal ﬂ ow signals in all intracranial vessels. Transforaminal examination demonstrated normal ﬂ ow in the BA and the left V4-VA segment. A retrograde ﬂ ow with reduced velocity was seen in projection of the right V4-VA segment (Fig. B19.8,

Fig. B19.9, Fig. B19.10).

Conclusion

Dissection in the right V2-VA segment with suspected distal VA occlusion, below the origin of the PICA. Retrograde ﬁ lling of the right V4-VA segment.

Conventional Angiography

Suspected Diagnosis

Cerebellar ischemia in the right PICA territory caused by right distal VA occlusion.

Questions to Answer by Ultrasound Techniques

• Was there occlusion or near-occlusion of the right VA?

• What was the exact location of the suspected occlu-

sion?

• Was there evidence of dissection?

Digital subtraction angiography (DSA) of the cervical, cerebral, and renal vessels was performed to further analyze the vascular pathology and to search for evidence of ﬁ bromuscular dysplasia (FMD). The right VA showed distinct variations in caliber commencing at the entrance of the V2-VA into the transverse foramen. A ﬁ liform ste- nosis was seen in the distal V2 segment with complete occlusion in the distal V3 segment. The left VA showed an “intimal ﬂ ap” in the central aspect of the V2 segment. The BA was normal. Retrograde ﬂ ow to the distal part of the right V4-VA segment was seen. The remaining intracranial vessels were normal and there was no evidence of FMD in the renal arteries (Fig. B19.11, Fig. B19.12, Fig.B19.13).

340 Case 19 Bilateral Extracranial Vertebral Artery Dissection with Distal Occlusion of the Right Vertebral Artery

Fig. B19.1 Cerebral MR FLAIR image, axial plane. Subacute large cerebellar ischemic lesion in the right PICA territory.

V2-VA-L

Fig. B19.3 Extracranial duplex, longitudinal plane. Left V2-VA diameter 3.9 mm.

Clinical Course

Fig. B19.2 3D TOF-MRA, coronal maximal intensity projection

(MIP). Absent signal in the distal right VA. Only a small signal i n d i c a t e s t h a t a l a r g e r v e s s e l i s m i s s i n g ( a r r o w h e a d ) . N o t e t h e m i s s ing P1-PCA (arrow) on the right side indicating fetal-type variant of PCA.

V2-VA-L

Fig. B19.4 Extracranial duplex, longitudinal plane. Normal left V2-VA ﬂ ow signal (ﬂ ow velocity 54/27 cm/s).

Final Diagnosis

The clinical development of the right-sided cerebellar syndrome changed the diﬀ erential diagnosis from a ves- tibular neuropathy to a cerebellar ischemia. On the basis

Right-sided PICA infarction caused by spontaneous right-sided occlusion of the VA proximal to the PICA ori-

gin in bilateral extracranial VA dissection. of our subsequent ﬁ ndings a spontaneous VA dissection was assumed. Initially intravenous partial thromboplastin time (PTT)-guided heparinization was commenced, which was later changed to oral anticoagulation with phenprocoumon. The patient was discharged with mild right hemiataxia. Follow-up MRI 6 months later showed no new ischemic events, and cervical MRA revealed a persisting VA occlusion. Clinically the patient had further improved. Treatment was changed to long-term antiplatelet therapy with aspirin. Ehlers–Danlos syndrome was excluded by a skin biopsy.

Discussion

Clinical Aspects

Here we discuss a 29-year-old woman who had acute ver-

tigo in combination with nausea and vomiting, leading to

the initial diagnosis of a left-sided vestibular neuropathy.

However, detailed neurologic examination on the follow-

ing day revealed additional mild cerebellar signs consist-

ing of spontaneous and gaze-evoked nystagmus to the

341Discussion

V2-VA-R

Fig. B19.5 Extracranial duplex, longitudinal plane. Large anechoic zone in the right V2-VA probably reﬂ ecting mural hematoma (arrowheads). Residual vessel lumen 2.6 mm. Note the regular proximal V2-VA diameter of ~3 mm.

V2-VA-R

Fig. B19.6 Extracranial duplex, longitudinal plane. Residual perfused lumen of the right V2-VA further distal is 1.7 mm.

V4-VA-L

Fig. B19.7 Extracranial duplex, longitudinal plane. High-resistance

ﬂ ow signal with low and short systolic ﬂ ow and completely absent diastolic ﬂ ow component in the right V2-VA suggestive of VA occlu- sion below the PICA origin (ﬂ ow velocity 15/0 cm/s).

right, a right-sided drift, and an impaired suppression of vestibular nystagmus; the head thrust test was normal on both sides. MRI subsequently conﬁ rmed subacute cere- bellar ischemia within the PICA territory.

Dizziness and vertigo are common but unspeciﬁ c symptoms which might be caused by several diseases seen in the ﬁ elds of general internal medicine, ENT, or neurology. It is not uncommon that a neurologic patient is treated with presumed gastroenteritis and myocardial infarction before being attended by a neurologist. Even in neurologic wards, in cases of acute vertigo, diﬀ eren- tiation between peripheral and central vestibular causes may be diﬃ cult. Cerebellar and, in particular, PICA infarc- tions might clinically present with the symptoms of a peripheral vestibular syndrome. The PICA supplies the key regions of the vestibulocerebellar system with its connections to the ipsilateral vestibular core regions, which may result in a predominantly vestibular pattern of PICA failure. Signs of ataxia may be faint or even absent. Up

Fig. B19.8 TCCS (tra nsfor amin al appr oach ). Norm al ﬂ ow signal in the left V4-VA (ﬂ ow velocity 55/38 cm/s).

to 17% of patients with PICA infarction present with the clinical symptoms of a pure vestibular neuropathy (Lee et al 2006). Even the horizontal head impulse test (head thrust maneuver) may be pathologic, wrongly indicating a peripheral vestibulopathy. Normal head impulse test, direction–changing nystagmus, and skew deviation (vertical ocular misalignment) on the other side had 100% sensitivity and 96% speciﬁ city for stroke in 101 examined patients with acute vestibular syndrome. In the case of a pathologic head impulse test a skew deviation may ﬁ - nally conﬁ rm a central vestibular syndrome (Kattah et al 2009, Tarnutzer et al 2011). In case of any doubt, cerebral MRI should be performed, so that cerebellar stroke is not missed (Savitz et al 2007).

In the case presented here, PICA infarction was the result of a distal VA occlusion caused by spontaneous extracranial bilateral VA dissection. An arterial dissection is an important diﬀ erential diagnosis that needs to be con- sidered as it is a cause of stroke in young patients in up to

342 Case 19 Bilateral Extracranial Vertebral Artery Dissection with Distal Occlusion of the Right Vertebral Artery

V4-VA-R

Fig. B19.9 TCCS (tra nsforam inal approach ). Re trogr ade ﬂ ow signal in projection of the right V4-VA (ﬂ ow velocity 25/11 cm/s).

Fig. B19.10 TCCS (trans foraminal app roach). N orma l ﬂ ow signal in the BA at a depth of 81 mm (ﬂ ow velocity 60/32 cm/s).

Fig. B19.11 DSA, right VA injection, posteroanterior view. Variations in caliber in the V2-VA and long-segmented ﬁ liform stenosis in its distal V2-VA part and proximal V3-VA segments, suggestive of dissection (arrowheads). Note several small branches connecting the VA with muscle arteries indicating a severely compromised ﬂ ow to the distal right VA (arrows).

25% of cases (Schievink 2001). A dissection may occur as a result of an intimal lesion with subsequent bleeding and development of an intramural hematoma within the layers of the arterial vessel wall. A more subintimal location will result in a narrowing of the vessel lumen or occlusion while a more subadventitial location results in the development of aneurysms. Further potential risk factors in our patient were the history of migraine and a recent upper respiratory tract infection (for further discussion on migraine, see Case 6). Recent infection, predominantly of the upper respiratory tract, has been associated with cervical artery dissection. In a study of young stroke patients (<50 years of age), recent infection was signiﬁ cantly more

Fig. B19.12 DSA, right VA injection, posteroanterior view, follow-up, late-phase DSA image of the area shown in Fig. B19.11 showing complete interruption of ﬂ ow within the distal V3-VA segment (arrowhead).

common in patients with vessel dissection (58.1% versus

32.8%; Grau et al 1999). Similar results were found in a study that compared 47 dissection patients (31.9%) and 52 patients with stroke of other etiology (13.5%) (Guillon et al 2003).

VA dissection present some diﬀ erences compared

with dissections of the internal carotid artery (ICA). In a study of 982 patients, the mean age and male proportion were slightly lower in VA lesions (41 versus 46 years and 51% versus 60%). Recent infection was less common (15% versus 22%), whereas trivial neck trauma was more often observed (37% versus 29%). Neck pain and ischemic stroke were more common (66% versus 39% and 77%

Fig. B19.13 DSA, left VA injection, posteroanterior view. Intimal

ﬂ ap mild dilatation in the left mid V2-VA segment (arrowhead).

343Discussion

10%. Subarachnoid hemorrhage was a rare event, occurring in only 2% of cases (Arnold et al 2006a). Compared with ICA dissections, pain seems to be less severe and more easily mistaken for being musculoskeletal in origin (Silbert et al 1995).

Therapeutic options for VA and ICA dissections are similar. Nowadays anticoagulation, initially with intravenous heparinization followed by 3–6 months of oral anticoagulation or antiplatelet therapy, can be considered as equivalent (for further reading on therapy, see Case 11). The risk of developing hemodynamic ischemic events is usually negligible because of the potential collateralization via the contralateral VA. In our case with bilateral VA involvement, a secondary vessel occlusion would have worsened the blood supply of the posterior circulation substantially as no posterior communicating artery (PCoA) was seen on the right side and a fetal-type PCA, incapable of participating in collateral ﬂ ow, was present on the left side. In our patient, the left VA remained occluded whereas the right VA normalized. Vessel restitution has been reported in up to 71% of cases (Bartels and Flügel

1996). VA dissecting aneurysms regress more frequently compared with the ICA (Touzé et al 2001).

versus 60%). Bilateral vessel aﬀ ection was also more often present in VA dissection (16% versus 10%). No obvious differences between VA and ICA dissections were noted with regard to headache (65% versus 68%), transient ischemic attack (TIA) (21% versus 20%), vessel occlusion (33% versus 34%) and wall hematoma (78% versus 83%) (Debette et al 2011).

Another potential risk factor for VA dissection is chiropractic manipulation. Typical movements are rotation, lateral ﬂ exion, ﬂ exion, extension, or a combination of these. The V3-VA segments run an elongated course surrounding the atlantoaxial joint. Here, cervical rotation is maximal and may lead to vessel stretching. A causative role of cervical manipulative therapy in VA dissection has been hypothesized for a long time. Reports that 30% of patients with VA dissection had prior cervical spine manipulation compared with 6% with ICA dissection support this assumption. Usually a short time delay between manipulation and clinical symptoms has been observed, varying from seconds up to 10 days (Dziewas et al 2003).

Our patient denied prior chiropractic treatment. Also, the site of dissection in the V2 segment and the bilateral appearance argues against a symptomatic cause. No evidence of systemic vascular disease or FMD was seen on DSA. Ehlers–Danlos syndrome was considered but excluded by a skin biopsy.

Spontaneous VA dissection without clinical symptoms is rare. In a recent study of 195 VA dissections in 169 patients, 92% were symptomatic. The remaining patients had complaints originating from additional symptomatic ICA dissection. Neck pain and/or headache, predominantly reported on the aﬀ ected side, were present in 84% of all cases and in 88% of patients with stroke. Vertigo, along with for head and neck pain, is the most prominent sign in VA dissection with an incidence of 57% (Saeed et al 2000). Cerebral infarction occurred in 67% and a TIA in

Angiologic and Anatomic Aspects

Most spontaneous VA dissections occur extracranially. The exact location where VA dissection starts depends on its course and the relationship between mobile and ﬁ xed vessel segments. Anatomically, the VA is ﬁ xed at its origin from the subclavian artery (SA), its passage through the spinal transverse foramen, and at its entry through the dura mater. The segments in between are mobile. Transitional segments between mobile and ﬁ xed parts are considered particularly prone to injury and are therefore the starting points of vessel dissection which usually lead to long-segmented downstream vessel changes. Data on the precise anatomic localization of VA dissections is contradictory, which can mainly be explained by diﬀ erent approaches to deﬁ ning the site of involvement. From a pathophysiologic point of view the beginning of the vessel injury rather than the maximal or distal extension of the hematoma should be considered as the site of dissection. Applying this deﬁ nition in 195 dissections, DSA or MRI analysis has shown VA dissections of 20%, 35%, and 34% within the V1, V2, and V3 segments, respectively (Arnold et al 2006a). Extracranial VA dissections seldom extend into the intracranial segments (Anson and Crowell 1991, Caplan et al 1988). A small proportion of VA dissections arise only intracranially. In the study by Arnold and coworkers, 79% of VA dissections had an extracranial location, 10% extended into the intracranial VA, and only 11% had an exclusive intracranial location (Arnold et al 2006a, Dziewas et al 2003). Extracranial duplex ultrasound is particularly sensitive in localizing VA dissections within the entry zone of the V1-VA segment into the transverse foramen at C6 and within the V3-VA segment.

The most frequently observed VA pathology in dissection is stenosis (56%), followed by occlusion (38%) and dissecting aneurysm with stenosis (6%) (Arnold et al 2006a). Comparable data was reported in a smaller study

344 Case 19 Bilateral Extracranial Vertebral Artery Dissection with Distal Occlusion of the Right Vertebral Artery

with 42% stenoses, 47% occlusions, and 12% normal ﬁ nd- ings using DSA, CTA, or MRA (Dziewas et al 2003). The above distribution is therefore quite similar to the pattern of the ICA dissections (Dziewas et al 2003, Pelkonen et al

2003). As in ICA dissection, an involvement of the VA can be

diagnosed noninvasively by ultrasound, MRI, and CTA techniques; conventional DSA has lost most of its importance. As the VA is, at least in young subjects, readily accessible along most of its extracranial course, sonographic diagnosis should be attempted searching for direct morphologic criteria at known preferential sites—the V1- to V2-VA transition and V3-VA at the atlas arch. At the entry zone of V1- to V2-VA, Bartels and Flügel (1996) were able to identify VA dissections in 11 of 26 dissections (42%) by detecting an increase in vessel diameter. Further typical ﬁ ndings are an irregular stenosis, a thick- ened hypo- or isoechoic vessel wall (indicating the intramural hematoma), a double lumen, and/or a dissecting aneurysm (Bartels and Flügel 1996, Lu et al 2000, Touboul et al 1988). There have not been any large extensive studies evaluating and comparing the importance of the above dissection criteria. Considering both direct and indirect signs, the reported sensitivity of ultrasound to detect VA dissection ranges from 66% to 100% (Auer et al 1998, Bartels and Flügel 1996, de Bray et al 1997, Pugliese et al 2007). For further reading, see also Chapter 5, “Dissection” under “Arterial Pathology.”

In young slim patients like our case, the examination

of the VAs is usually not problematic. Therefore, B-mode sonography was able to reveal a hypoechoic zone within the V2-VA segment, probably corresponding to the mural hematoma. However, in elderly people and in patients with a large neck circumference, B-mode quality may not be suﬃ cient to directly detect the dissection-related ves- sel wall changes. In these cases, indirect hemodynamic signs may be of help as they are indicative of stenosis or occlusion. Increased or decreased ﬂ ow velocities may be found depending on the length and degree of lumen narrowing. In distal occlusion, high-resistance ﬂ ow signals are seen in the proximal vessel segments as demonstrated in our case. However, indirect hemodynamic criteria do not help in distinguishing between occlusion caused by dissection, embolism, or atherosclerosis. Also, VA hypoplasia and anatomic variations might lead to diﬃ cul- ties in interpretation of ultrasound ﬁ ndings. Analysis of the V2-VA vessel diameter and blood ﬂ ow may be of help. In hypoplasia, at least a small diastolic ﬂ ow should be preserved. In case of a normal VA diameter the observed V2-VA ﬂ ow alterations depend on the location of the VA occlusion. Extracranial V3 occlusion or intracranial V4 oc-

clusion proximal to the PICA origin will, as in our case, result in a distinct high-resistance ﬂ ow signal without a diastolic ﬂ ow component. A “stump” signal is rarely ob- served in distal VA occlusion proximal of the PICA origin because of its typical connection to small arteries of the neck muscles. In this type of occlusion, retrograde ﬁ lling of the distal V4-VA segment, ensuring blood ﬂ ow into the PICA, might be observed. A V4-VA occlusion distal of the PICA origin might result in normal V2-VA signals or only mildly reduced diastolic ﬂ ow velocities (see also Chap- ter 5, “VA Occlusion” under “Extracranial Pathology”). As V2-VA insonation alone carries the risk of missing a distal V4-VA occlusion or high-grade stenosis, complete insonation of all VA segments including the intracranial V4-VA segments should be performed whenever pathology in the posterior circulation is suspected.

The value of neuroradiologic methods has already been discussed in relation to ICA dissections (see also Case 11). In VA dissection, MRI veriﬁ cation of the intra- mural hematoma may be more diﬃ cult than it is with ICA dissection, as the vessel diameter is smaller and the VA often follows a more tortuous course, particularly within the V3-VA segment. Also, the signal of the vertebral vein could be mistaken for a wall hematoma. A r n o l d a n d c o w o r k e r s r e p o r t a s u c c e s s r a t e f o r d i a g n o s i s of 91% (Arnold et al 2006a). In our case, no speciﬁ ed MRI was performed to detect a mural hematoma. If done, the time-dependent change in MRI blood sensitivity should be considered: Within the ﬁ rst day or two, the hema- toma often appears isointense to the surrounding body tissue, especially in T1-weighted sequences. From day 3 up to 2 months, a distinct increase in the signal can be seen which subsequently fades and disappears over a period of ~6 months (Paciaroni et al 2005). Early MRI, in our case performed on day 2, might therefore fail to detect the hematoma and a repeated scan might have to be c o n s i d e r e d .

TOF-MRA alone is not suitable for detecting VA dissection. The reported sensitivity in a very small group of ﬁ ve VA dissections was 20%; the speciﬁ city was 100% (Levy et al 1994). With regard to multislice CTA, a retrospective study in 17 patients with VA dissection and 17 controls using DSA as reference reported a sensitivity of 100%, speciﬁ city of 98%, and positive and negative predictive values of 95%, and 100%, respectively (Chen et al 2004b). These excellent results were recently conﬁ rmed by a second study in 15 patients yielding values of 100%, 95%, 93.7%, and 100%, respectively (Pugliese et al 2007). A comparison of duplex ultrasound with CTA by the same group yielded values of 66%, 60%, 55.5%, and

70.5%, respectively.

Case 20

Right Internal Carotid Artery Dissection with Fast Recanalization

345

Clinical Presentation

A 56-year-old man presented with progressive paresis of his left arm. Three days prior to presentation, he had experienced some pain on the right side of his neck and headaches while exercising in a gym for the ﬁ rst time. The following day, he observed clumsiness of his left hand and drooping of his right eyelid. The left-sided paresis continued to progress, at which stage he presented to the hospital emergency department. The patient had no known vascular risk factors. The neurologic examination revealed a mild left-sided sensorimotor hemiparesis and Horner’s syndrome on the right side (National Institute of Health Stroke Scale [NIHSS] score: 3).

Initial Neuroradiologic Findings

Cranial CT on the day of admission revealed multiple hypodense areas in the right middle cerebral artery (MCA) territory. MRI conﬁ rmed multiple ischemic lesions within the internal border zone region of the right hemisphere. Axial images demonstrated a reduced ﬂ ow void in the right carotid siphon. Time-of-ﬂ ight MR angiography (TOF-MRA) depicted an absent signal of the right distal internal carotid artery (ICA) and a bilateral partial fetal-type posterior cerebral artery (FT-PCA) origin (Fig. B20.1 and Fig. B20.2).

Doppler spectrum analysis showed a high pulsatility in the right common carotid artery (CCA) and a highresistance ﬂ ow signal in the right ICA with a low and short systolic ﬂ ow and completely absent diastolic ﬂ ow com- ponent, indicative of either near-occlusion or occlusion of the ICA below of the origin of the ophthalmic artery (OA). External carotid artery (ECA) Doppler spectra were normal (Fig. B20.3, Fig. B20.4, Fig. B20.5, Fig. B20.6; see also Video

B20.1 ).

Transcranial Duplex Sonography

The right M1-MCA segment presented a marked poststenotic ﬂ ow pattern. The A1 segment of the anterior cerebral artery (A1-ACA) yielded a retrograde ﬂ ow, also with severe poststenotic alterations. The anterior communicating artery (ACoA) was not visualized. Elevated ﬂ ow velocities were seen in the right P1-PCA segment (125/69 cm/s), here with an obviously turbulent ﬂ ow pattern, and in the left A1-ACA segment (150/75 cm/s), both indicative of collateral ﬂ ow to the right anterior cir- culation via the ACoA and the posterior communicating artery (PCoA). The left MCA and PCA, in addition to the distal right P2-PCA segment, demonstrated normal ﬂ ow. No ﬂ ow was detected in the OA on the right side. The ﬂ ow signal of the left OA was normal (Figs. B20.7–B20.12; see also Video

B20.1).

Suspected Diagnosis

Right internal border zone infarction (BZI) caused by ICA dissection and secondary ICA occlusion.

Questions to Answer by Ultrasound Techniques

• Was there evidence of dissection?

• Was there a real occlusion or high-grade stenosis of the ICA?

• If so, what were the intracranial collateral pathways?

Evaluation of Collateral Function

Cerebrovascular Reactivity Testing

Intravenous administration of 1 g acetazolamide during continuous transcranial Doppler (TCD) monitoring of both M1-MCA segments revealed a 60.6% increase in ﬂ ow velocity on the left side and a 1.6% increase in ﬂ ow velocity on the right (Fig. B20.13) (see also Chapter 3, “Acetazolamide Infusion Test” under “Metabolic Coupling”).

Ultrasound Delay Testing

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode imaging was normal. There were no atherosclerotic changes and no signs of proximal ICA dissection.

After intravenous administration of a 3-mL sonographic contrast bolus (Levovist, 300 mg/dL) and continuous monitoring of both M1-MCA Doppler spectra, a rightsided, 1-second delay of bolus arrival was observed (Fig. B20.14) (see also Chapter 3, “Ultrasound Delay Test” under “Metabolic Coupling”).

346 Case 20 Right Internal Carotid Artery Dissection with Fast Recanalization

Fig. B20.1 (A) MR T2-weighted image, axial plane. Multiple hyperintense signals within the right internal border zone (arrows), indicative of hemodynamic infarction. (B) MR T2-weighted image, axial plane (magniﬁ ed view). Absent ﬂ ow void within the right-sided cav- ernous ICA segment, suggestive of reduced or absent intraluminal ﬂ ow (arrow). Note the contralateral normal ﬂ ow void signal of the ICA and of the BA in front of the pons (arrowheads).

CCA-L

Fig. B20.3 Extracranial duplex, longitudinal plane. Normal left CCA

ﬂ ow (ﬂ ow velocity 87/28 cm/s).

Fig. B20.2 Intracranial 3D TOF-MRA, axial maximal intensity projection (MIP). Signal loss of the right ICA indicating high-grade ﬂ ow reduction or occlusion. Note the bilateral fetal-type PCA (arrowheads). Both P1-PCA segments are hardly visible. Note also the reduced signal in the right MCA (arrows) and in the right A1-ACA (arrows) indicating compromised postocclusive ﬂ ow (arrows)

CCA-R

Fig. B20.4 Extracranial duplex, longitudinal plane. High-resistance

ﬂ ow signal in the right CCA (peak-systolic ﬂ ow velocity 63 cm/s).

Conclusion

Suspected right distal ICA dissection with near-occlusion or occlusion proximal to the OA origin. Exhausted CVR and insuﬃ cient collateral pathways supplying the right MCA territory via the ACoA and the ipsilateral PCoA.

and partially via a hypoplastic right P1-PCA segment providing retrograde blood ﬂ ow into the right MCA via the FT-PCA and antegrade blood ﬂ ow into the distal PCA segments. Filling of the right MCA territory was delayed. These ﬁ ndings were consistent with a near-oc- clusion of the right ICA due to vessel wall dissection (Figs. B20.15–B20.20).

Conventional Angiography

Fig. B20.21 shows a schematic of the patient’s extra-

and intracranial brain-supplying arteries.

Digital subtraction angiography (DSA) demonstrated a long segmental irregularity in the right ICA with a

Clinical Course (1)

cone-shaped high-grade stenosis starting 5 cm above the carotid bifurcation and extending to the vertical segment of the petrous C6-ICA segment. Only residual and delayed contrast ﬁ lling was seen in the distal ICA. Collateralization mainly occurred via the ACoA

Intravenous heparin, aiming for a twofold increase of partial thromboplastin time (PTT) was started. TOF-MRA 2 weeks later demonstrated a normalized right ICA signal.

347Clinical Course (2)

ICA-L

Fig. B20.5 Extracranial duplex, longitudinal plane. Normal ﬂ ow sig- nal in the left ICA (ﬂ ow velocity 79/40 cm/s).

M1-MCA-L

ICA-R

Fig. B20.6 Extracranial duplex, longitudinal plane. High-resistance

ﬂ ow signal in the right ICA with a low and short systolic, and completely absent diastolic ﬂ ow component indicative of near-occlu- sion or occlusion of the ICA below the OA origin.

M1-MCA-R

Fig. B20.7 TCC S (trans temporal a ppro ach), left -sided i nson ation, midbrain plane. Normal left M1-MCA ﬂ ow (ﬂ ow velocity 69/31 cm/s). Note the prominent left blue-coded signal indicating ﬂ ow away from the probe and toward the P2-PCA corresponding to a fetal-type PCA seen in MRA (arrow).

Follow-up Neurosonologic Findings (Day 20)

Extracranial Duplex Sonography

A normalized ﬂ ow pattern was seen in the right CCA and ICA compared with the contralateral side (Fig. B20.22,

Fig. B20.23, Fig. B20.24, Fig. B20.25).

Transcranial Duplex Sonography

The right M1-MCA and A1-ACA as well as the PCA segments demonstrated normalized ﬂ ow velocities and pulsatility. A ﬂ ow within the hypoplastic right

Fig. B20.8 TCCS (transtemporal approach), right-sided insonation. Poststenotic ﬂ ow pattern in the right M1-MCA (ﬂ ow velocity 54/38 cm/s).

P1-PCA segment was no longer detectable (Fig. B20.26, Fig. B20.27, Fig. B20.28, Fig. B20.29, Fig. B20.30).

Conclusion

Flow normalization in all insonated vessels indicating a rapid resolution of the right ICA dissection.

Clinical Course (2)

The patient was switched to oral anticoagulation with phenprocoumon and was discharged with a mild left- sided hemiparesis. Anticoagulation was stopped 6 months later. Until that time no further clinical events had occurred and the left hemiparesis had completely resolved.

348 Case 20 Right Internal Carotid Artery Dissection with Fast Recanalization

A1-ACA-L

Fig. B20.9 TCCS (tran stemporal appro ach) , left -sid ed ins onati on. Increased nonturbulent ﬂ ow in the left A1-ACA, indicative of collat- eral ﬂ ow (ﬂ ow velocity 150/75 cm/s).

SCA-L

A1-ACA-R

Fig. B20.10 TCCS (transtemporal approach), right-sided insonation. Retrograde, poststenotic ﬂ ow pattern in the right A1-ACA (ﬂ ow velocity 45/35 cm/s).

P1-PCA-R

Fig. B20.11 TCCS (transte mporal appr oach ), lef t-sid ed i nson ation . Normal ﬂ ow in the left superior cerebellar artery (SCA) (ﬂ ow veloc- ity 50/20 cm/s). Note again the prominent left blue-coded PCoA with ﬂ ow toward the P2-PCA indicating fetal-type PCA. In fetal-type PCA only a weak ﬂ ow signal may be detected if a P1-PCA is present. Because of the almost normal ﬂ ow signal the SCA was assumed.

Final Diagnosis

Right internal BZI after distal ICA dissection with subsequent near-occlusion and initially insuﬃ cient collateral blood ﬂ ow via the ACoA and the retrogradely perfused ipsilateral FT-PCA. Rapid vascular normalization within 3 weeks.

Discussion

Clinical Aspects

Here we report of a 56-year-old man who presented several notable features in relation to his spontaneous ICA dissection:

• Dissection occurred while he was exercising in a gym.

• Cerebral imaging revealed a right internal BZI but no territorial infarction.

Fig. B20.12 TCCS ( transte mpor al ap proa ch), rig ht-s ided in sona tion. Turbulent signal and increased ﬂ ow velocity in the right P1-PCA (ﬂ ow velocity 125/69 cm/s) indicating a hypoplastic vessel (func- tional stenosis). Note the red-coded right-sided vessel signal considered to be a fetal-type PCA with a paradoxical ﬂ ow direction toward the ICA because of the steno-occlusive lesion of the ICA (arrow).

Velocity (cm/s)

150

100

10:05

Fig. B20.13 Acetazolamide infusion test, bilateral TCD monitoring of M1-MCA ﬂ ow. Exhausted CVR in the right MCA. Note a marked diﬀ er- ence between the right and left sides, with an increase in ﬂ ow velocity of 60.6% on the left side and 1.6% on the right after 15 minutes.

10:10 10:15 10:20

MCA-L + 60.6%

MCA-R + 1.6%

Time (min)

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