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Fig. B20.14 Echo contrast delay test, bilateral

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.

TCD monitor ing of M1-MC A ﬂ ow, revealing a delay of 1 second on the right side. Top: right MCA, bottom: left MCA. Note the signal enhancement of the Doppler spectrum caused by the inﬂ ow of the intravenous Levovist echo contrast bolus at ~12 seconds on the left (black arrow) and at 13 seconds on the right side (white arrow).

349Discussion

Fig. B20.15 DSA, right CCA injection (early arterial phase), lateral

view. Dissecting string sign with suspected proximal ICA occlusion with a large stump (arrow).

• The ﬁ rst dissection-related symptoms occurred ~24 hours prior to the development of focal neurologic deﬁ cits, which then further progressed over several days.

• The dissection completely recanalized within 20 days.

Fig. B20.16 DSA, right CCA injection (late arterial phase), lateral view. Filling of an irregularly shaped ICA starting at the mid-carotid region (arrows). The distal ending of the stenosis reaches the vertical part of the petrous ICA (arrow).

exercise, particularly in untrained subjects, can indeed considered to be a risk factor for dissection. Much like the patient in Case 11, this patient had insuﬃ cient collater- alization via the cerebral arterial circle (circle of Willis) leading to hemodynamic failure and subsequent internal BZI. In spontaneous ICA dissection, territorial infarction

is a frequent ﬁ nding but BZI is rare. In a large series in- Like the patient in Case 11, this patient’s dissection occurred in a gym. Most such patients, on careful recollection, will similarly report a suggestive “minor trauma” to which the dissection could potentially be attributed (Fisher et al 1978, Luken et al 1979). Excessive physical

cluding 131 ICA dissections in 130 patients, BZI was pres-

ent in 5% of cases but all of them had concurrent embolic

lesions (Benninger et al 2004) (for further discussion on

BZI, see also Chapter 4, “Border Zone Infarction” under

“Arterial Ischemia,” and Case 30).

350 Case 20 Right Internal Carotid Artery Dissection with Fast Recanalization

Fig. B20.18 DSA, left ICA injection (early arterial phase), posteroanterior view. Cross-flow from the left ICA to the right MCA. Note the delayed MCA territory filling of the right MCA (proximal M2 segment) compared with the left MCA (opercular M3 segment).

Fig. B20.17 DSA, right CCA injection (late arterial phase), posteroanterior view. Delayed MCA contrast ﬁ lling on the right side (arrows). Note that no A1-ACA vessel is visualized.

Fig. B20.19 DSA, left ICA injection (capillary phase), posteroanterior view. More obviously delayed right-sided circulation in the capillary phase. Note the parenchymal phase on the left hemisphere but only insular MCA branch ﬁ lling on the right side (arrowheads).

Our patient’s ﬁ rst dissection-related symptoms occurred 1 day before he developed focal neurologic signs. Such a time delay is often observed in spontaneous ICA dissection. A study in 42 stroke patients with ICA dissection reported prior local signs or transient ischemic attack (TIA) in 79% of cases. The time delay ranged from

Fig. B20.20 DSA, right vertebral artery (VA) injection, posteroanterior view. Note the contrast ﬁ lling of right insular MCA branches (arrows) via a small P1-PCA (arrowhead).

minutes up to 31 days. However, in 82% of patients, stroke occurred in less than 1 week (Biousse et al 1995). This time span seems to indicate the greatest embolic activity of the dissected vessel wall.

Finally, our patient presented rapid and complete

r e c a n a l i z a t i o n . V e s s e l r e s t i t u t i o n o c c u r s i n t h e m a j o r i t y

CCA-L

351Discussion

Fig. B20.21 Schematic of the patient’s extra- and intracranial brain-supplying arteries. High-grade right distal ICA stenosis ( c i r c l e ) . T h e r e i s c o l l a t e r a l b l o o d ﬂ ow toward the right MCA and right ACA territory via ACoA and retrograde blood ﬂ ow toward right A1-ACA. Additional blood ﬂ ow is from the posterior circulation via a right hypoplastic P1-PCA into the right MCA despite the presence of a partial fetal-type PCA.

CCA-R

Fig. B20.23 Extracranial duplex, longitudinal plane. Normalized right CCA ﬂ ow (ﬂ ow velocity 89/22 cm/s).

Fig. B20.22 Extracranial duplex, longitudinal plane. Normal left CCA ﬂ ow (ﬂ ow velocity 108/32 cm/s).

ICA-L

Fig. B20.24 Extracranial duplex, longitudinal plane. Normal ﬂ ow signal in the left ICA (ﬂ ow velocity 62/24 cm/s).

of cases, but in most it ﬁ nalizes after 3 months. Gradual vessel restitution can, however, start immediately, as could be demonstrated by serial duplex ultrasound examinations (Steinke et al 1994) (for further discussion on spontaneous dissection, see Case 11).

extracranial ICA ﬂ ow signal. In this patient the diastolic ﬂ ow component was missing, which clearly points toward a major distal ﬂ ow obstruction (occlusion/near-occlusion) proximal to the OA origin. A residual diastolic ﬂ ow would have argued in favor of a high-grade stenosis or occlusion/ near-occlusion distal from the OA origin.

Although most ischemic events associated with cervi-

Angiologic and Anatomic Aspects

A near-occlusion of the distal ICA is a diagnostic challenge for all imaging modalities. In contrast to proximal ICA near-occlusion, which can usually be evaluated by duplex ultrasound, a conﬁ dent diagnosis of a distal near-occlu- sion is problematic. However, a diﬀ erentiation between occlusion/near-occlusion and the presence of a highgrade stenosis can be achieved by evaluating the proximal

cal artery dissection are of embolic origin, patients with a resulting high-grade stenosis or dissection-related ICA occlusion might show ipsilateral hemodynamic events in up to 16% of cases (Steinke et al 1996). Of particular interest is to ﬁ nd out which patient with a high-grade stenosis is at particularly high risk of developing hemodynamic ischemic stroke. The ﬁ rst diagnostic signs of insuﬃ cient collateralization were observed in early an- giographic studies by showing a delayed ipsilateral MCA

352 Case 20 Right Internal Carotid Artery Dissection with Fast Recanalization

ICA-R M1-MCA-L

Fig. B20.25 Extracranial duplex, longitudinal plane. Normalized

ﬂ ow signal in right ICA (ﬂ ow velocity 58/21 cm/s).

M1-MCA-R

Fig. B20.27 TCCS (transtemporal approach), right-sided insonation. Normalized right M1-MCA ﬂ ow (ﬂ ow velocity 72/27 cm/s).

contrast ﬁ lling (Boczko and Caplan 1967, Krayenbühl and Yasargil 1982).

Standard ultrasound parameters for measuring the quality of existing collaterals in ICA occlusion are the ﬂ ow velocity and pulsatility, the systolic ﬂ ow acceleration in the ipsilateral MCA, and cerebrovascular reactivity (CVR) (Hartmann et al 2000, Kelley et al 1990, Markus and Cullinane 2001, Ringelstein et al 1988). CVR measurement is well-established and probably one of the most frequently used functional tests to assess the risk of hemodynamic stroke. In our case we performed the acetazolamide infusion test which revealed an ipsilateral exhausted CVR, indicating insuﬃ cient intracranial collateral function.

More recently, other ultrasound methods of collateral function assessment have been described. One of these is the ultrasound-based “delay test” performed in our patient (see Fig. B20.14) which parallels the angiographic delay studies described above (see also Chapter 3, “Ultrasound Delay Test” under “Metabolic Coupling”). This test analyzes the hemodynamic eﬀ ects of an extracranial high-grade carotid stenosis or occlusion by simultaneous ultrasonographic MCA echo-contrast bolus tracking (Gómez-Choco

Fig. B20.26 TCCS (transte mporal appr oach ), lef t-sid ed i nson ation . Normal left M1-MCA ﬂ ow (ﬂ ow velocity 102/39 cm/s).

A1-ACA-L

Fig. B20.28 TCCS (transte mporal appr oach ), lef t-sid ed i nson ation . Normalized left A1-ACA ﬂ ow (ﬂ ow velocity 85/35 cm/s).

et al 2015). It directly evaluates the quality of the ACoA, PCoA, or OA in ﬁ lling the MCA of the aﬀ ected side. It can be assumed that delayed arrival of the contrast agent is directly related to an increased ﬂ ow resistance and small diameter of the above-mentioned vessels. In healthy volunteers, the maximal observed diﬀ erence between the left and right sides as assessed by this technique is

0.48 seconds. Our patient had a delay of 1 second, which is clearly outside the physiologic range. Although prospective clinical data is not yet available, the combination of impaired CVR and a pathologic delay test—each analyzing diﬀ erent aspects of the cerebral hemodynamics—proba- bly indicates an increased risk of hemodynamic ischemic events. Also, a DSA-based delay test has been rediscovered. Yamamoto and coworkers (2004) compared the angiographic time delay of contrast bolus arrival between the carotid siphon and maximal staining of the capillary bed in 28 patients with occlusive ICA or MCA disease. Bilateral diﬀ erences (i.e., delays) were analyzed and results compared with acetazolamide single photon emission CT (SPECT). The authors found a good correlation between the techniques. Patients with poor CVR yielded delays of

353Discussion

A1-ACA-R

Fig. B20.29 TCCS (transtemporal approach), right-sided insonation. Normalized right A1-ACA ﬂ ow now revealing an antegrade ﬂ ow direction (ﬂ ow velocity 74/30 cm/s).

up to 2 seconds compared with 1.18 seconds, in those with preserved CVR.

Other potentially useful techniques in patients with occlusive disorders of the ICA are delay analyses with contrast-enhanced MRI (Apruzzese et al 2001, Trivedi et al 2005) or contrast-enhanced CT (Matsumoto et al 2007, Waaijer et al 2007), both using bilateral comparison of mean transit time data. Also, noncontrast dynamic spin labeling MRA has successfully been used (Bokkers et al 2008, Warmuth et al 2005). With the implementation of noninvasive 4D cerebrovascular imaging, using either CT or MRI, more precise information about hemodynamic severity of steno-occlusive diseases as well as the quality of collateral ﬂ ow and other parameters such as the clot burden has become available (Kortman et al 2015, Parmar et al 2009).

Also, intracranial ﬂ ow measurements using 4D phase-contrast MR angiography have been reported as a valid alternative in vessel segments that are technically diﬃ cult to assess by TCD, e.g., the carotid siphon (Meckel et al 2013).

In all the above techniques a delay of 0.5–1.5 seconds can be detected in patients with severe steno-occlusive disorders of the ICA if no suﬃ cient collateral pathways are present (see also Chapter 3, “Ultrasound Delay Test” under “Metabolic Coupling”). Patients with chronically impaired collateral function are at particularly high risk of developing a future TIA or stroke. Treatment strategies

P2-PCA-R

Fig. B20.30 TCCS (transtemporal approach), right-sided insonation. Normal ﬂ ow in the right P2-PCA (ﬂ ow velocity 62/26 cm/s). A P1-PCA ﬂ ow signal was no longer detectable.

might therefore need to be adapted and individualized. In high-grade ICA stenosis a carotid endarterectomy (CEA) or stenting might be advisable. In ICA occlusion an EC–IC bypass operation might be necessary (see also Case 25).

Finally, our case demonstrated the special constellation of a bilateral fetal-type PCA, with a paradoxical reversed ﬂ ow through a hypoplastic P1-PCA segment which was clearly visible on the MRA images. However, although MRA only demonstrated a weak connecting vessel toward the basilar artery (BA), ultrasound revealed a turbulent ﬂ ow in a small P1-PCA segment toward the distal PCA and the MCA territory, conﬁ rmed on DSA im- aging. The excess ﬂ ow within this P1-PCA segment was easy to detect by transcranial color-coded sonography (TCCS) and considered as functional stenosis. After vessel recanalization and ﬂ ow normalization no signal was any longer detectable in the hypoplastic P1-PCA segment. The observed cross-ﬂ ow via the ACoA was impaired not only because of a small ACoA lumen and probably also a small lumen of the right A1-ACA segment, but also because of reduced ﬂ ow from the left ICA, which was also providing blood ﬂ ow to the left ACA, MCA, and PCA terri- tories. This probably explains the dramatic hemodynamic impairment in this patient. It is important to note that a functional stenosis may be present not only in the ACoA and PCoA but also in the P1-PCA and A1-ACA segments in hypoplastic variants. For further discussion on DSA, MRI, and CT angiography (CTA) in ICA dissection, see Case 11.

354

Case 21

Mid-basilar Artery Occlusion Due to Intracranial Dissection

Clinical Presentation

A 33-year-old woman acutely developed left-sided weakness and drowsiness. In the days preceding presentation she had had an occipital headache of moderate severity. She had no relevant medical history and no known vascular risk factors. In particular, she had no history of migraine. Neurologic examination revealed an impaired level of consciousness, a left-sided hemiparesis, and gaze deviation to the left (National Institute of Health Stroke Scale [NIHSS] score: 17).

Initial Neuroradiologic Findings

Initial CT 6 hours after onset of symptoms showed normal ﬁ ndings, in particular no signs of subarachnoid hem- orrhage (SAH). Assuming a diagnosis of basilar artery (BA) disease, emergency digital subtraction angiography (DSA) was performed, which revealed a severe narrowing of the middle segment of the BA including an “intimal ﬂ ap” sug- gestive of BA dissection. Perfusion of the posterior cerebral artery (PCA) territory was maintained by the BA (not shown). No interventional treatment was performed.

Suspected Diagnosis

tine regions, and cerebellar hemispheres, the latter being considered to present infarctions in the territories of the anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA) (Fig. B21.1). 3D time-of-ﬂ ight MR angiography (TOF-MRA) demonstrated absence of ﬂ ow signals in the middle segment of the BA (Fig. B21.2).

Questions to Answer by Ultrasound Techniques

• Was there an embolic source in the extracranial segments of the vertebral arteries (VA)?

• Was there occlusion or high-grade stenosis of the BA?

• Was there impaired ﬂ ow in both PCAs?

Initial Neurosonologic Findings (Day 3)

Extracranial Duplex Sonography

Examination of the carotid arteries revealed normal results. The diameter of both V2-VA segments was within the normal range (left 3.6 mm, right 4.4 mm). Doppler spectrum analysis showed reduced ﬂ ow velocity and a mildly increased pulsatility in both VAs (Fig. B21.3 and Fig. B21.4).

Brainstem ischemia in the vertebrobasilar territory caused by BA dissection.

Clinical Course (1)

Heparinization was commenced with the aim of achieving a partial thromboplastin time (PTT) that was double the normal value. Her mental status improved. Clinical follow-up 2 days later demonstrated left hemiataxia and mild left hemihypesthesia. In addition the patient had right-sided hemianopia and severe dysarthria, both of which had initially been masked by her impaired consciousness.

Follow-up Neuroradiologic Findings (Day 3)

An MRI scan taken 2 days after admission revealed multiple ischemic lesions in the vertebrobasilar territory, particularly in the left occipital lobe, left thalamus, bilateral pon-

Transcranial Duplex Sonography

Normal ﬂ ow signals were found in both middle (MCA) and anterior (ACA) cerebral arteries. Increased velocities and turbulent ﬂ ow were detected in the right pos- terior communicating artery (PCoA). The right P1-PCA segment and the top of the BA demonstrated a reversed ﬂ ow signal while the P2-PCA segment was normal. The left P1-PCA segment revealed a stenotic ﬂ ow signal (ﬂ ow velocity 124/83 cm/s). Turbulence, mildly increased ﬂ ow velocities (systolic ﬂ ow velocity ~90 cm/s), and reduced pulsatility were seen throughout the left P2- and P3PCA segments, suggestive of postischemic hyperemia caused by the large PCA infarction. Digital tapping of the right internal carotid artery (ICA) yielded positive oscillation eﬀ ects in both PCAs and in the retrograde BA conﬁ rming collateral blood ﬂ ow from the right ICA via the right PCoA toward the posterior circulation (Figs. B21.5–B21.11). Transforaminal insonation revealed reduced ﬂ ow velocities in both V4-VA segments, compa- rable with the extracranial ﬁ ndings. There was a distinct- ly reduced ﬂ ow signal in the proximal BA but there was

355Clinical Course (2)

Fig. B21.1 MR diﬀ usion-weighted image (b = 1,000), axial plane.

Hyperintense signals bilaterally in the cerebellar hemispheres and pons (A) as well as in the left occipital lobe and thalamus (B).

V2-VA-L

Fig. B21.3 Extracranial duplex, longitudinal plane. Reduced ﬂ ow velocity and mild increased pulsatility in the left V2-VA with a diameter of 3.6 mm (ﬂ ow velocity 37/13 cm/s, PI = 1.1).

no signal more distally, despite the presence of excellent insonation conditions. Intravenous echo contrast administration (5 mL Levovist, 300 mg/dL) conﬁ rmed the absence of distal basilar ﬂ ow. A prominent signal was seen in the both AICAs and in the right posterior inferior cerebellar artery (PICA) (Fig. B21.12, Fig. B21.13, Fig. B21.14, Fig. B21.15).

Fig. B21.2 3D TOF-MRA. Circle of Willis, sagittal maximal intensity projection (MIP). Absent ﬂ ow signal in the mid-segment of the BA (arrowhead). Note that no prominent PCoA is visible.

V2-VA-R

Fig. B21.4 Extracranial duplex, longitudinal plane. Identical ﬂ ow signal in the right V2-VA revealing a diameter of 4.4 mm (ﬂ ow velocity 37/13 cm/s).

as well as retrograde ﬁ lling of the distal BA with sup- ply of both SCAs. A left P1-PCA stenosis was not visible (Fig. B21.16, Fig. B21.17, Fig. B21.18, Fig. B21.19). A schematic of the patient’s extra- and intracranial brain-supplying arteries is shown in Fig. B21.20.

Conclusion

Mid-BA occlusion distal to the AICA origin. Collateral blood ﬂ ow toward both PCAs and the upper BA segment from the right ICA via the right PCoA. In addition, suspected left-sided P1-PCA stenosis, probably caused by a partially resolved embolus.

Clinical Course (2)

Because of the long time delay and the large areas of infarcted brain parenchyma, no interventional treatment was considered. The etiology of the BA dissection with secondary occlusion remained unclear. There was no history of trauma and no ﬁ ndings suggestive of vas- culitis or inﬂ ammatory vessel disease. Fibromuscular dysplasia (FMD) had been excluded by DSA, and lab-

Conventional Angiography (Day 4)

DSA on the next day conﬁ rmed mid-BA occlusion distal to the AICA origin, with collaterals via the right PCoA

oratory data had ruled out coagulopathy. On extensive cardiologic examination, no source of embolism was found. Because of the intracranial location, treatment was changed from heparin to aspirin. Three weeks after

356 Case 21 Mid-basilar Artery Occlusion Due to Intracranial Dissection

MCA-R

PCoA-R

ICA-R

Fig. B21.5 TCCS (t rans tempo ral approach) , right -sid ed in sona tion, midbrain plane. Circle of Willis with prominent right-sided PCoA (arrow). Note the retrograde ﬂ ow in the right blue-coded P1-PCA (arrowhead).

P2-PCA-R

PCA-R

PCA-L

Fig. B21.6 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Doppler spectrum analysis in the right PCoA. Functional stenosis with increased velocit y and turbulent ﬂ ow (ﬂ ow velocity 173/100 cm/s).

P1-PCA-L

Fig. B21.7 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Positive oscillation eﬀ ect in the right P2-PCA caused by slight tapping of the right extracranial ICA (arrows; ﬂ ow velocity 30/20 cm/s).

admission the patient was transferred to a rehabilitation clinic, awake and with moderate left-sided hemiataxia, right-sided hemianopia, and cerebellar dysarthria. After 6 months the patient had remained stable with regression of the ataxia and dysarthria. Ultrasound examination showed unchanged signs of BA occlusion but complete regression of the left P1-PCA stenosis (not shown).

Final Diagnosis

Spontaneous BA dissection with secondary persistent mid-BA occlusion distal to the AICA origin and consecutive multiple embolic infarcts within the vertebrobasilar artery territory.

Fig. B21.8 TCCS (tr anst emporal appro ach) , left -sided insonati on, midbrain plane. Increased ﬂ ow velocity in the left P1-PCA (ﬂ ow velocity 124/83 cm/s). Note the positive oscillation eﬀ ect in the left P1-PCA caused by slight tapping of the right extracranial ICA (arrows). Note also the retrograde red-coded ﬂ ow signal in the right P1-PCA (arrow).

Discussion

Clinical Aspects

Here we describe a 33-year-old woman who sustained multiple infarcts within the posterior circulation. A spontaneous BA dissection was diagnosed, leading to secondary BA occlusion and causing in-situ thrombotic and artery-to-artery embolic infarctions.

There are no detailed epidemiological data on the incidence and prevalence of intracranial dissections. An intracranial dissection is a rare cause of stroke, and rare in comparison to extracranial dissections. In a recent Chinese study 1.5% of all ischemic strokes were related to intracranial dissections. A perforator-related stroke was the most often assumed cause in one-third of patients. As

357Discussion

P3-PCA-L

Fig. B21.9 TCCS (tr anst emporal appro ach) , left -sided insonati on, thalamic plane. Low-pulsatility turbulent ﬂ ow with increased veloc- ity in the left distal P3-PCA (ﬂ ow velocity 87/53 cm/s).

V4-VA-L

Fig. B21.10 TCCS (transtemporal approach), right-sided insonation, upper pontine plane. Assumed distal segment of the BA demonstrating retrograde ﬂ ow. Note the positive oscillation eﬀ ect during slight tapping of the right extracranial ICA (arrows).

V4-VA-R

Fig. B21.11 TCC S (transfor aminal appr oach) . Red uced ﬂ ow signal in the left V4-VA (ﬂ ow velocity 37/21 cm/s).

main radiologic signs, MRI and MRA revealed an intima ﬂ ap or double lumen in 44% and a dissecting aneurysm in 13% of cases (H. Chen et al 2015). Smaller case series and single case reports suggest that predominantly younger patients between 30 and 50 years of age and more males than females are aﬀ ected, at least in vertebral dissection (Basseti et al 1994, Caplan et al 1988). In the posterior circulation, dissections most frequently occur in the V4-VA segment, close to the PICA origin, but may also affect primarily the PICA itself (Matsumoto et al 2014). An extension into the BA might also be seen, but isolated BA dissections are extremely rare (Alexander et al 1979).

The underlying mechanism of extracranial and intracranial dissection is thought to be similar. After an intimal tear, blood can enter the wall of the artery leading to subintimal vessel wall hematoma that is more prone to stenosis and occlusion. Alternatively, a subadventitial lesion may lead to the formation of a dissecting aneurysm more prone to rupture and subarachnoid bleeding. Intracranial arteries have thinner medial and adventitial layers than extracranial arteries, and lack an external

Fig. B21.12 TCCS ( tran sfora mina l appr oach) . Reduced velo city in the right V4-VA (ﬂ ow velocity 30/15).

elastic lamina. Therefore, these vessels more frequently develop aneurysms and carry a subsequent risk of SAH (O’Connell et al 1985). Dissection-induced SAH with a vessel lesion between the medial and adventitial layers has been seen in 79% of cases in an autopsy study (Yamaura and Ono 1994).

In contrast to the posterior circulation, the anterior

circulation is more frequently aﬀ ected in children and young adults (Schievink et al 1994b). Here, dissections are most frequently found in the intracranial ICA. Approximately 100 cases have been reported in the English literature so far. The most frequent location is the supraclinoid C1/C2-ICA segment, from which the dissection often extends into the proximal MCA and ACA (Chaves et al 2002). Isolated MCA and ACA dissections may also occur. Until 2005 only 23 patients with MCA dissection had been reported (Lin et al 2005) (for further discussion on MCA dissection, see also Case 24). In ACA dissection, ischemic stroke is often related to A2-ACA segment involvement and SAH to A1-ACA involvement (Ohkuma et al 2003).

358 Case 21 Mid-basilar Artery Occlusion Due to Intracranial Dissection

AICA-L

Fig. B21.13 TCCS (trans foraminal a ppro ach). P romi nent ﬂ ow sig- nal in the left AICA at a depth of 75 mm (ﬂ ow velocity 45/25 cm/s).

Fig. B21.14 TCC S (tr ansforami nal app roac h). The color -mod e i mage reveals a prominent right-sided PICA, AICA, and proximal BA but no distal BA signal. Note the color gap over 15 mm. The distal blue-coded signal at a depth of 95 mm most likely belongs to the anterior part of the circle of Willis and not to the distal BA. A retrograde BA ﬂ ow signal cannot be demonstrated.

Fig. B21.16 DSA, left VA injection, lateral view. Mid-basilar occlusion. Note the cone-shaped occlusion of the BA (arrowhead), suggestive of dissection.

Fig. B21.15 DSA, left VA injection, posteroanterior view. Mid-basilar occlusion (arrowhead). Note the prominent right PICA (arrow).

The causes of intracranial dissections are not clearly established. Mechanical injuries such as are found in the extracranial system seem far less likely, as intracranial arteries are less mobile and are not adherent to bone. Another possible explanation is the presence of an arteriopathy that may lead to vessel wall instability. For instance, Ehler–Danlos syndrome and ﬁ bromuscular dysplasia are associated with spontaneous dissections, although with a clear preference for the extracranial a r t e r i e s ( S c h i e v i n k 2 0 0 1 , S c h i e v i n k e t a l 1 9 9 4 a ) . R e l e v a n t diﬀ erential diagnoses for a dissecting stenosis are ather- osclerosis, radiation-induced vasculopathy, and fusiform and blister-like aneurysms.

The clinical presentation of extra- and intracrani-

al dissections is diﬀ erent. In intracranial dissections, unilateral severe headaches are almost always present. Furthermore, the interval between dissection and the manifestation of clinical symptoms tends to be shorter (Zweiﬂ er et al 2004). Often, the extent of the neurologic deﬁ cit ﬂ uctuates within the ﬁ rst 2 weeks, which has been attributed to hypoperfusion induced by vessel lumen reduction (Hart and Easton 1983). In posterior circulation dissection large or multiple posterior circulation strokes may occur (Caplan et al 1988). As with extracranial dissection, migraine is a common ﬁ nding in intracranial spontaneous dissection.

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