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306
Case 26
Extracranial Vertebral Artery Dissecting Aneurysm
following Basilar Artery Stenting
Clinical Presentation
A 58-year-old man was admitted to an external hospital
with right-sided sensorimotor hemisyndrome and dysarthria. Several weeks earlier he had complained of transient vertigo and a gait disorder. The patient had known
vascular risk factors of arterial hypertension, hypercholesterolemia, and diabetes mellitus. On admission he presented fluctuating symptoms with a moderate proportional hemiparesis, hemihypesthesia on the right side,
and dysarthria (National Institute of Health Stroke Scale
[NIHSS] score 7).
Initial Neuroradiologic Findings
The initial cerebral computed tomography (CT) scan
showed hypodensities in both cerebellar hemispheres
and a small hypodense area in the right pons consistent
with subacute infarction (Fig. B26.1). Diffusion magnetic
resonance imaging (MRI) revealed moderate acute left
paramedian pontine ischemia (Fig. B26.2).
Suspected Diagnosis
Recurrent ischemia in the vertebrobasilar artery territory
suspicious of basilar artery (BA) stenosis or thrombosis.
Conventional Angiography
Digital subtraction angiography (DSA) demonstrated a
high-gradestenosisinthemiddlesegmentoftheBA.The
vertebral and carotid arteries were normal (Fig. B26.3).
Clinical Course (1)
In view of the remitting clinical symptoms, and the lesions
on MRI, interventional percutaneous transluminal angioplasty of the BA followed by stent implantation was performed via the left vertebral artery (VA). The procedure
was technically and clinically successful and a follow-up
CT scan showed a patent BA without evidence of bleeding
or new ischemic lesions (Fig. B26.4). Secondary stroke
prevention was commenced with aspirin and clopidogrel
and the patient was referred to a rehabilitation center. By
this stage there had still not been any neurosonologic
examination.
Two weeks following the stenting, the patient had a
transient ischemic attack (TIA) with double vision and a
left-sided hemiparesis that lasted a few hours. Furthermore, the residual right-sided hemiparesis and the dysarthria mildly worsened. The patientwas then admitted to
our department for the first time.
Questions to Answer by Ultrasound Techniques
• Was there restenosis or occlusion of the stented BA?
• Was there evidence of an embolic source in the verte-
brobasilar system?
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode imaging of the carotid arteries showed moderate
atherosclerotic vascular changes, more pronounced in the
carotid bifurcation. Doppler spectrum analysis demonstrated normal findings. The left VA showed a marked
increase in caliber in the V2-VA segment at the vertebral
level between C5 and C6 with a maximal diameter of
10.5mm in B-mode and color-mode imaging. The diameter of the V1-VA segment was 5.5 mm. A constant diameter
ranging from 4.3 mm to 4.5 mm was seen in all segments of
the right VA. The Doppler spectrum analysis demonstrated
normal flow signals in the left middle and distal V2-VA
segment as well as in the right V2-VA segment (Figs.
B26.5–B26.10).
Transcranial Duplex Sonography
Transtemporal insonation yielded normal findings in the
anterior (ACA),middle (MCA), and posterior (PCA) cerebral
arteries on both sides. Transforaminal insonation demonstrated normal flow signals in the BA and the intracranial
segment of both VAs (not shown).
Conclusion
Suspected left VA dissection with formation of a dissecting
aneurysm in the proximal V2-VA segment at the C5/C6
level. There were no signs of detectable restenosis in the
stented BA.
Cranial CT and CTA (Day 1)
Cranial CT confirmed the known cerebellar and pontine
infarctions. In addition, a new paramedian pontine infarct
of moderate size was seen on the right side adjoining the
BA stent (Fig. B26.11). Computed tomographic angiography (CTA) confirmed the widening of the left V2-VA
segment between C5 and C6 in terms of a VA dissecting
aneurysm (Figs. B26.12, B26.13).
Final Diagnosis
307
Degree of Neurosonologic Difficulty: High
Clinical Course
The VA dissection was thought to be of iatrogenic origin
generated during the initial DSA with BA stent implantation. The recent pontine infarction was attributed to a
stent-related secondary occlusion of a perforating artery.
An embolic event, potentially originating from the aneurysm could not be excluded. Therefore, oral anticoagulation with phenprocoumon was started and the patient was
referred again to a rehabilitation center. He was then lost
to follow-up.
Final Diagnosis
Primary left-sided pontine infarction and old right-sided
pontine and cerebellar infarctions caused by BA stenosis of
unknown origin. Secondary right-sided pontine infarction
aftersuccessfulBAstentingeitherinducedbysecondary
occlusion of a pontine perforator artery within the stented
region or by artery-to-artery embolism from V2-VA segment dissecting aneurysm.
Fig. B26.1 Unenhanced cranial CT, axial plane. Hypodensities in the
right cerebellar hemisphere and a small right-sided hypodense area
within the pons suggestive of subacute stroke (arrows). Note the
enlarged and slightly hyperdense BA (arrowhead).
Fig. B26.2 MRI, apparent diffusion coefficient (ADC) map, axial
plane. Acute left-sided paramedian pontine ischemic lesion (arrow).
Case 26 Extracranial Vertebral Artery Dissecting Aneurysm following Basilar Artery Stenting
308
Degree of Neurosonologic Difficulty: High
Fig. B26.3 DSA, left VA-injection, posteroanterior view. High-grade
stenosis in the middle segment of the BA (arrow).
Fig. B26.5 Extracranial duplex, longitudinal plane (B-mode). Left
V1-VA diameter: 5.5 mm.
Fig. B26.4 Intracranial CTA, 3D-reconstruction. Patent BA after
stenting (arrows).
Fig. B26.6 Extracranial duplex, longitudinal plane (B-mode): Left
V2-VA dilatation between the transverse processes of C5 and C6
with a diameter of 10.5 mm (encircled by arrows) suggestive of
dissecting aneurysm.
Final Diagnosis
309
Degree of Neurosonologic Difficulty: High
Fig. B26.7 Extracranial duplex, longitudinal plane. Color-coded im-
age of the dilated left V2-VA between C5 and C6 with a diameter of
10.8 mm.
Fig. B26.9 Extracranial duplex, longitudinal plane. Normal diameter
of the right V2-VA segment (4.4 mm).
Fig. B26.8 Extracranial duplex, longitudinal plane. Normal flow in
the distal left V2-VA between C3 and C4 (flow velocity: 49/17 cm/s).
Fig. B26.10 Extracranial duplex, longitudinal plane. Normal flow in
the right V2-VA (flow velocity: 43/13 cm/s).
Fig. B26.11 Unenhanced cranial CT, axial plane. New right-sided
hypodense area within the pons adjacent to the BA stent (arrow).
Note the hyperdensity within the BA caused by the stent itself
(arrowhead).
Fig. B26.12 CTA, curviplanar reformatted image, coronal view.
Widening of the left V2-VA between C5 and C6 consistent with
dissecting aneurysm (arrow).
Case 26 Extracranial Vertebral Artery Dissecting Aneurysm
310
Degree of Neurosonologic Difficulty: High
Fig. B26.13 CTA, curviplanar reformatted image, lateral view: Wid-
ening of the left V2-VA between C5 and C6 consistent with dissecting aneurysm (arrowhead).
Discussion
Clinical Aspects
The case illustrates a complex vertebrobasilar pathology.
Our 58-year-old patient suffered from multiple episodes of
cerebral ischemia in the posterior circulation, involving
the cerebellum and the pons. The underlying cause was
an isolated high-grade mid-basilar stenosis. An endovascular stent successfully treated the stenosis. However,
postintervention, the patient sustained another episode
of pontine infarction on the contralateral side either
caused by a perforating artery occlusion or an artery-toartery embolic event from the extracranial VA dissecting
aneurysm.
The largest register of prospectively collected data, from
407 patients with ischemia of the posterior circulation, is
the New England Medical Center Posterior Circulation
Registry (NEMC-PCR) (Caplan et al. 2004). Of the 407
patients, 87 demonstrated a BA stenosis > 50 % or occlusion, mostly of atherosclerotic origin. Isolated occlusive
processes within the BA were observed in approximately
45 % of cases and the mid-basilar segment was affected in
about 62 % of cases. Classic vascular risk factors such as
hypertension or hyperlipidemia were common. Clinically,
66 % of these patients suffered from posterior circulation
TIAs. More than half of these subsequently evolved to
completed stroke with a preferential location within the
pons in about 76% of cases.
Contrary to previous beliefs, the NEMC-PCR does show
that the clinical outcome after brain ischemia caused by BA
processes might be relatively good. This might in part be
explained by the improved imaging modalities which are
able to also depict lessdistinct findings. In this series 72.2 %
of patients had a good clinical outcome. A poor clinical
outcome has been associated with involvement of the
distal territory, emboli and BA occlusions as well as an
initial impaired consciousness (Voetzsch et al. 2004). In
our case, it is likely that an atherosclerotic BA stenosis was
present. This hypothesis is supported by the multiple
known vascular risk factors, the observed atherosclerotic
ICAvesselwallchanges,andtheclinicalpresentationwith
recurring TIAs and subsequent pontine and cerebellar infarctions.
The acute therapy of BA occlusive processes is already
discussedincase8(forfurtherreadingseealsocase8,
p.165). Treatment of ischemic stroke due to BA stenosis
consists of a number of medical and interventional approaches. However, no randomized trials have addressed
this issue. As anticoagulation was not shown to be superior
in the treatment of intracranial stenoses, the primary
medical treatment concept is inhibition of thrombocyte
function (Chimowitz et al. 2005) (for further reading see
also case 5 p.149).
Finally, patients who suffer from recurrent ischemia
despite the use of the best medical treatment might profit
from an endovascular intervention. In a small case series of
12 symptomatic patients with stent placement in the BA,
no periprocedural stroke or death occurred (Gomez et al.
2000). Meanwhile three large multicenter trials have been
published on the treatment of symptomatic intracranial
stenoses, including the posterior circulation, with a stent
especially designed for intracranial use. The SSYLVIA study
referred about 61 treated patients, 17 of them presenting
BA stenosis. The primary success rate was high but after 6
months, 32 % of the intracranial stents showed a restenosis
> 50 %. No detailed information regarding results of BA
stenting was given. A further technical advance is the
recently introduced wingspan stent, a self-expandable
and not a balloon-expandable stent system, as was used
in the SSYLVIA study. Two groups have reported their
experiences with the wingspan stent system. In the first
study,stentplacementforBAstenosiswasperformedin
nine of 45 patients (20 %), but detailed information about
the results in this subgroup was not given (Bose et al.
2007). The second study included 14 out of 78 patients
(18%) with a BA stenosis. The reported general periprocedural complication rate was high and included five deaths
(6.1 %). Three of the patients who died had BA stenosis,
resulting in a mortality rate of 21 % for BA intervention.
Two of these patients died from vessel rupture, the third
from extended infarctions (Fiorella et al. 2007) (for further
discussion on intracranial stenting, see also Case 5, p.149).
Early stent occlusion,dissectionsat the stent border,and
occlusion of perforator arteries are further potential complications associated with stent placement. The risk of
perforater-related stroke is particularly high in patients
who already present perforator-related infarctions before
intervention compared with those with other types of
infarct (8.2 % vs. 0.8 %). Most infarcts, however, occur during or on the day of the intervention (Jiang et al. 2006).
Discussion
311
In our case, two complications occurred despite the
successful placement of the stent itself. The new pontine
infarction, directly located near the stent was probably
caused by a delayed stent-related perforator occlusion 2
weeks after the interventional procedure. Furthermore,
the large dissecting aneurysm in the proximal left V2-VA
segment was also considered to be intervention-related as
the left VA wasthe access path for BA stenting. The location
at the vessel entry into the first transverse foramen is a
typical finding in extracranial VA dissection (for further
discussion on VA dissection, see also Case 19, p. 245). It is
worthnotingthatourpatientdidnotreportabouttypical
neck pain. In VA dissections, however, pain may be absent
inupto12%ofcases(Arnoldetal.2006a).
Treatment of dissecting aneurysms is still a matter of
debate. Formerly, oral anticoagulation was often initiated
because of a suspected high risk of arterial embolism.
Currently they are considered to be benign. In a group of
16patients with 20 dissecting ICA aneurysms, treated with
antiplatelet medication alone, no cerebral ischemia was
noted during a mean follow-up period of 37 months (Guillon et al. 1999). Similar results were found in a series of
nine VA aneurysms which resolved spontaneously in 80 %.
No aneurysm enlarged and no patient suffered from ischemia while taking antiplatelet treatment (Touzé et al. 2001).
Surgical or endovascular treatment is unnecessary and
might lead to cerebral ischemia or vessel occlusion (Kadkhodayan et al. 2005). It should therefore be restricted to
patients in whom antithrombotic therapy fails or in whom
an enlargement of aneurysm becomes obvious (for further
reading see also case 11).
Angiologic and Anatomic Aspects
Dissecting aneurysms have been reported to occur in 10 %
to 46 % of cases with VA dissection and in 13 % to 48 % of
cases with ICA dissection (Touzé etal.2001).Thehigh
variability reflects inconsistent definitions used by different angiologic methods. It is also attributed to the varying
examination points in time as an aneurysm can be missed
in the acute phase of dissection, for example, during an
initial vessel occlusion. With duplex ultrasound, aneurysms may easily be overlooked or not even be detectable.
Bartels and Flügel (1996) found one distal V2-VA aneurysm
in 15 patients (7 %) with angiographically confirmed VA
dissection. To optimize the diagnostic sensitivity of ultrasoundinsuspectedVAdissectionanddissectinganeurysm, examination should consist of imaging of the total
visible extracranial artery from V0 to the V3 segment,
paying special attention to the known dissection-prone
vessel regions such as the entry site of the VA into the
bony canal of the transverse processes.Positive ultrasound
findings may be the presence of vessel lumen enlargement
in B- and color-mode with or without flow signal alterations. A bidirectional Doppler flow pattern may be seen
within a nonthrombosed aneurysm, similar to that which
can be seen physiologically in a large carotid sinus. If
detected, follow-up should concentrate on the further
evolution and normalization of the vessel lumen.
In comparison to duplex ultrasound, MRA and CTA are
clearly superior techniques in the diagnosis and follow-up
of dissecting aneurysms of the brain-supplying arteries.
Although no systematic studies have addressed this specific question, results from observational studies indicate
that beside the DSA technique, multislice CTA is the most
sensitive method, followed by contrast-enhanced magnetic resonance angiography (MRA) and time-of-flight
(TOF) MRA. Contrast-enhanced MRA revealed three aneurysms missed in TOF MRA (Touzé etal.2001).CTAmay
identify dissecting aneurysms not diagnosed by MRI and
TOF MRA (Elijovich et al. 2006) (for further discussion on
ultrasound and neuroimaging of VA dissection, see also
Case 19, p. 245).
Degree of Neurosonologic Difficulty: High
312
Case 27
Diffuse Cerebral Angiomatosis
Clinical Presentation
A 30-year-old woman was admitted to our department
following a generalized epileptic seizure. After recovery,
shegaveaseveralyears’ history of chronic throbbing
headaches that were frequently accompanied by nausea
and vomiting.More recently, she had developed left-sided
hyperacusis, gradually worsening bilateral pulsatile tinnitus, impaired visual acuity, and recurrent transient leftsided hemiparesis, each of which lasted up to 3 hours. Her
medical history had been unremarkable until she was 13
years old, at which stage a periorbital bruit, left-sided
retinal edema, and retinal hemorrhages were incidentally
discovered. Cranial computed tomography (CCT) performed at this time was reported to be normal. She remained asymptomatic until the age of 22, when a right
central retinal venous thrombosis led to marked visual
impairment in addition to a focal seizure with a left-sided
hemisyndrome. Subsequently she developed symptomatic focal epilepsy and was prescribed carbamazepine.
The frequency of seizures increased after the birth of her
daughter and changed to predominantly generalized epilepsy.
Physical examination on admission revealed bilateral
periorbital pulsatile bruits, a reduced right-sided visual
acuity, a bilateral retinal angiomatosis, a left-sided inner
ear deafness, and a mild left-sided sensorimotor hemiparesis.
Initial Neuroradiologic Findings
Cerebral magnetic resonance imaging (MRI) on the day of
admission revealed no ischemic lesions but did demonstrate multiple pathologic vessel signals with a right-sided
predominance as well as right hemispheric brain atrophy.
Intracranial contrast-enhanced magnetic resonance angiography (MRA) showed multiple dilated, pathologic vessels with right-sided predominance (Figs. B27.1, B27.2).
Suspected Diagnosis
Bihemispheric arteriovenous malformation (AVM).
Questions to Answer by Ultrasound Techniques
• Which were the arterial feeders and venous drainage
vessels?
• Can a multimodal assessment be made of cerebral hemodynamics including the measurement of global cerebral blood flow (gCBF), cerebral circulation time (gCCT),
and cerebral blood volume (gCBV)?
Initial Neurosonologic Findings
Extracranial Duplex Sonography
B-mode ultrasound revealed no atherosclerotic vascular
changes. Doppler spectrum analysis showed normal and
symmetric flow signals, but velocities were generally increased in all extracranial arteries and also in the internal
jugular veins (IJVs) (Figs. B27.3–B27.8).
Transcranial Duplex Sonography
Transcranial color-coded sonography (TCCS) showed increased flow velocities (between 100 cm/s and 250 cm/s
systolic flow), low pulsatility indices (< 0.6), and moderately turbulent flow patterns in all basal cerebral arteries
(Figs. B27.9–B27.14).Inaddition,flowvelocitieswere
raised in the detectable cerebral venous vessels (not
shown).
Multimodal Assessment (gCBF, gCCT, and gCBV)
The gCBF, assessedas the sum of bloodvolume flowin both
internal carotid arteries (ICAs) and vertebral arteries (VAs)
was 2620 mL/min, which is approximately three times
higher than in healthy individuals. The gCCT was determined as the time-delay between the arrival of the contrast bolus at the extracranial ICA and its exit at the extracranial IJV following intravenous Levovist contrast bolus injection into an antecubital vein. In our patient, the
gCCT was significantly shortened (2.9 s, reference value:
7s) (Fig. B27.15). The calculated ultrasound-derived gCBV
(gCBF ×gCCT) was increased (126 mL, reference value:
80 mL) (see also Chapter 3, “Parameters of Cerebral Hemodynamics,” p. 60).
Final Diagnosis
313
Conclusion
Generalized increase of blood flow velocities and gCBF,
reduction of gCCT, and increase of ultrasound determined
gCBV suggestive of marked hyperemia, consistent with a
diffuse AVM on both hemispheres.
Conventional Angiography
Digital subtraction angiography (DSA) was performed to
search for AVM, feeding arteries, and draining patterns,
and to evaluate interventional therapeutic options. A diffuse, superficial cortical angiomatosis was seen on both
sides comprising numerous arteriovenous shunts leading
to early venous filling of the markedly dilated superficial
and deep cerebral veins (Figs. B27.16, B27.17).
Clinical Course
The character of the malformation, consisting of a diffuse
cortical angiomatosis without a classic AVM nidus and an
additional retinal angiomatosis, did not allow any inter-
ventional therapy. The malformation was considered to be
themostlikelycauseofthepatient’s signs of increased ICP
(headaches, nausea), epilepsy as well as of the mild leftsided hemiparesis. The hemiparesis was either a recurrent
Todd paresis or a result of transient hemodynamic steal
phenomena, caused by right-sided accentuation of the
malformation and the subsequent right-sided frontoparietal brain atrophy.
The anticonvulsant treatment with carbamazepine was
optimized and additional symptomatic treatment with
analgesics led to some reduction in headaches, nausea,
and vomiting. However, the patient continued to have
mild hemiparesis and epilepsy. It seems that the extent
of the malformation had progressed from age 13 but remained stable over the last year of follow-up as control
MRI and MRA did not suggest any remarkable changes in
the angiomatosis.
Final Diagnosis
Bilateral cortical and retinal angiomatosis. A rare undefined neurocutaneous syndrome was considered.
Degree of Neurosonologic Difficulty: High
Fig. B27.1 MR T2-weightedimage, axial plane. Numerous flow-void
signals with a right-sided predominance as a correlate of pathologic
arterial and venous vessels. Note the mild right-sided frontoparietal
cortical atrophy. (Reproduced from Schreiber et al. 2003, with kind
permission of Lippincott, Williams & Wilkins.)
Fig. B27.2 Intracranial contrast-enhanced 3D MRA, sagittal MIP.
Note multiple dilated arterial and venous vessels. (Reproduced
from Schreiber et al. 2003, with kind permission of Lippincott,
Williams & Wilkins.)
Case 27 Diffuse Cerebral Angiomatosis
314
Degree of Neurosonologic Difficulty: High
Fig. B27.3 Extracranial duplex, longitudinal plane. Increased flow
velocity (127/53 cm/s) and flow volume(530 mL/min) in theleft ICA.
Fig. B27.5 Extracranial duplex, longitudinal plane. Increased flow
velocity (103/48cm/s) and flow volume (390 mL/min) in the left VA.
Fig. B27.4 Extracranial duplex, longitudinal plane. Increased flow
velocity (125/58 cm/s) and flow volume (780 mL/min) in the right
ICA.
Fig. B27.6 Extracranial duplex, longitudinal plane. Increased flow
velocity (92/43 cm/s) and flow volume (280 mL/min) in the right VA.
Fig. B27.7 Extracranial duplex, longitudinal plane. Increased flow
velocity (40/28 cm/s) and volume flow (570 mL/min) in the left IJV.
Fig. B27.8 Extracranial duplex, longitudinal plane. Increased flow
velocity (59/38 cm/s) and volume flow (1170 mL/min) in the right
IJV.
Final Diagnosis
315
Degree of Neurosonologic Difficulty: High
Fig. B27.9 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased flow velocity in the left M1-MCA (flow
velocity: 234/129 cm/s).
Fig. B27.11 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased flow velocity in the left A1-ACA (flow
velocity: 200/124 cm/s).
Fig. B27.10 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Increased flow velocity in the right M1-MCA (flow
velocity: 247/176 cm/s).
Fig. B27.12 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Increased flow velocity in the right A1-ACA (flow
velocity: 109/65 cm/s).
Fig. B27.13 TCCS (transtemporal approach), left-sided insonation,
midbrain/thalamic plane. Increased flow velocity in the left P2-PCA
(flow velocity: 117/71 cm/s).
Fig. B27.14 TCCS (transtemporalapproach), right-sidedinsonation,
thalamic plane. Increased flow velocity in the right P3-PCA (flow
velocity: 96/61 cm/s).