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Case 17 Ascending Middle Cerebral Artery Occlusion
236
A recentstudy collected data on 64 HIV-positivepatients
(aged < 46 years) with ischemic stroke. In contrast with a
control group of age-matched stroke patients without HIV,
a subgroup of the HIV-positive patients demonstrated an
association with a recent or intercurrent infection within
the past 3 months in 37 %. These weremostly opportunistic
infections such as tuberculosis, varicella zoster, Pneumo-
cystis carinii pneumonia, and cryptococcal meningitis. An
analysis of the stoke etiology in the total study population
revealed that 28 % had an opportunistic infection-related
stroke (infectious meningitis/vasculitis) and 19 % had a
coagulopathy, of which 40 % were due to raised anticardiolipin antibodies. Cardiac embolism was found in 14%, and
HIV-associated vasculopathy in 20 %. Multiple etiologies
Degree of Neurosonologic Difficulty: Medium
were present in 11 % (Tipping et al. 2007). In a comparable
study including 77 patients with ischemic stroke with a
mean age of 42 years, the mechanism of stroke was large
artery atherosclerosis in 12 %, cardiac embolism in 18 %,
small vessel occlusion in 18 %, other determined etiology in
23%,andundeterminedorincompleteevaluationin29%.
Vasculitis was considered to lead to stroke in 10 patients
(13%) and hypercoagulability in seven patients (9 %). Protein S deficiency was detected in 10/22 (45 %) and anticardiolipin antibodies in 9/31 (29 %) examined patients
(Ortiz et al. 2007). Ahigh prevalence of proteinS deficiency
in HIV-positive stroke patients was described in earlier
studies (Qureshi et al. 1997). However, a recent comparison of HIV-positive patients with and without stroke
demonstrated that the protein S deficiency is rather an
epiphenomenon associated with the HIV infection itself
(Mochan et al. 2005). Strokes of cardioembolic origin are
associated with different variants of HIV-related cardiomyopathy (Cardoso et al. 1998). However, cardiac disease
is often found in late-stage HIV infection.
Different types of HIV vasculopathy, which may affect all
vessel sizes, have been described and are currently the
subject of intensive research. Small-vessel vasculopathy
is characterized by hyaline small-vessel thickening, perivascular space dilatation, rarefaction, and pigment deposition with vessel wall mineralization, and occasional perivascular inflammatory cell infiltrates. This type of vasculopathy is often clinically asymptomatic and leads to
microinfarctions (Connor et al. 2000). Affliction of middle-sized arteries can be detected by angiography. Multilocular degenerative ectasia involving the circle of Willis
(CW) and its proximal branches has also been reported. All
affected vessels can display aneurysmal and nonaneurysmal lesions with stenoses and occlusions or local thrombi
within the extra- and intracranial arteries (Berkefeld et al.
2000,Chetty et al. 2000,Nogueraset al. 2002,Tippinget al.
2006, Tipping et al. 2007). The complex pathogenesis of
HIV-related vasculopathies has not yet been solved.
The occurrence of atherosclerosis in HIV patients was
rare before the introduction of the protease inhibitors,
which was explained by the young age of the patients
andtheirreducedlifeexpectancy.Asthehighlyactive
anti-retroviral therapy (HAART) dramatically reduced the
early mortality associated with the disease, atherosclerosis became more relevant. Protease inhibitors induce a
number of metabolic effects. Their use may lead to hypertriglyceridemia and hypercholesterolemia, increased serum insulin and peptide C levels with proven insulin resistance, and peripheral lipodystrophy. Relevant alterations in blood lipids can be observed in 24–64 % of patients
treated with a protease inhibitor (Henry et al. 1998, Tsiodras et al. 2000). Possibly related to the above findings,
more and more studies report vascular events in young
HIV patients without classic vascular risk factors but
treated with protease inhibitors. An ultrasound study of
patients treated with protease inhibitors for at least 1 year
demonstrated an increased prevalence of atherosclerosis
in the carotid arteries. Atherosclerotic vessel wall changes
(plaque or IMT > 1 mm) were shown in 51 % of HIV patients
on protease inhibitor therapy and 15 % of HIV patients not
taking protease inhibitors. In the control group of matched
healthy volunteers only 7 % were affected (Maggi et al.
2000). A recently published study showed that combined
antiretroviral therapy is a predictor of subclinical atherosclerosis (Jerico et al. 2006). Menge and coworkers reported a patient on protease inhibitor therapy who, similar
to our patient, also had stepwise symptoms of ischemic
stroke over a few weeks. This was, however, caused by
rapid development of severe atherosclerotic changes
within the MCA and distal ICA (Menge et al. 2000). In our
patient, the combined antiretroviral therapy might have
promoted the development of extracranial atherosclerotic
vessel wall changes as other vascular risk factors were not
present. The uncommon accession of the intraluminal
thrombus with subsequent M1-MCA occlusion is probably
a result of a combination of the above trigger factors.
Angiologic and Anatomic Aspects
In our case, the proximal M1-MCA occlusion at the origin
of the artery from the ICA was visualized with all the
applied techniques (MRA, DSA, and transcranial colorcoded sonography [TCCS]) (for further discussion on neuroimaging in intracranial occlusion, see also Case 10,
p.176). An exact determination of the level of occlusion
is important for the evaluation of infarct volume and subsequent clinical outcome. Of particular interest is whether
the origins of the lenticulostriate arteries (LSAs) are also
affected. MCA occlusions can be divided into four types
(Saito et al. 1987):
• Type 1: proximal M1-MCA occlusion with or without the
involvement of the LSA.
• Type 2: distal M1 occlusion beyond the origin of the LSA.
• Types 3 and 4: occlusion of one or more M2-MCA
branches.
Our patient initially presented with probably a type 4 MCA
occlusion which later on progressed to a type 1 occlusion
(see also Chapter 5, “Intracranial Pathology,” p. 94).
Discussion
237
Another factor influencing the extent of infarction and
clinical outcome is the quality of the collaterals. For instance, a proximal M1-MCA occlusion might result in complete MCA territory or lenticulostriate infarction only, depending on the available collaterals. Even during thrombolysis, the efficacy of the leptomeningeal collaterals influences the final infarct volume, as they provide the blood
supply to the borderzone of the infarct,i. e.,the penumbra.
This function seems to be related to the perfusion pressure,
which is why a stable perfusion pressure, even if above
normalvalues,isdesired.Thishypothesisissupportedby
isolated case reports of patients in whom perfusion MRI
demonstrated that a controlled increase in blood pressure
reduces the size of the oligemic area (Hillis et al. 2003) (see
also Chapter 5, “Collateral Pathways,” p. 101). DSA is the
only valid method for direct visualization of the peripheral
and leptomeningeal collaterals, for example, retrograde
filling of cortical arteries or distal M2-MCA branches, as
has been shown in our case via the hyperperfused ACA.
Also, important PCA branches, e. g., the occipitotemporal
and the parietooccipital arteries, feeding the leptomeningeal collateral vessels, were identified.
TCCS in our patient also showed clear signs of leptomeningeal collateralization in the form of raised flow velocities in the anterior and posterior cerebral arteries. More
detailed ultrasound analysis also permits the identification of PCA branches, but this was not done in our patient
(see also Chapter 2, “Intracranial Arteries,” p.24). Over all,
leptomeningeal collateralization in our patient was rather
good, as the secondary proximal MCA occlusion only led to
a large striatal infarction with little cortical involvement.
Another indirect extracranial ultrasound sign of relevant
proximal MCA flow obstruction was the reduced flow
velocity in the normal-sized extracranial ICA, a common
finding in proximal MCA occlusion. However, a reduced
extracranial ICA flow signal is not a reliable indicator of
proximal MCA occlusion, and normal or nearly normal
extracranial ICA flow profiles may be found despite the
presence of MCA occlusion in cases with good leptomeningeal collateralization via the ACA in combination with
an ipsilateral fetal-type PCA (see also Ta b l e A 5 . 4 ,p.97).
The TOF MRA technique in our patient was able to demonstrate the M1-MCA occlusion later confirmed by DSA,
but was unable to evaluate the efficiency of collateral
function. With respect to the intracranial collaterals from
the anterior communicating and posterior communicating
arteries, TOF MRA has a negative predictive value of 53 %
compared with functional TCCS, and is therefore only of
limited value (Hoksbergen et al. 2003b). It may, however,
reveal a prominent PCA main stem as an indirect sign of
leptomeningeal collateralization on comparison of the affected and nonaffected sides (Uemura et al. 2004). This
phenomenon was also seen in our patient.
Degree of Neurosonologic Difficulty: Medium
238
Case 18
Bilateral Internal Carotid Artery Dissection
Clinical Presentation
A 45-year-old man presented with a 2-week history of
transient episodes of impaired visual acuity in the right
eye, tinnitus, and intermittent headaches. Furthermore, he
complained of nausea, vomiting, and vertigo. One week
before admission he had experienced an acute episode of
right-sided retroorbital pain. He had no vascular risk factors, except migraine. On admission neurological examination revealed no focal neurologic deficits. In particular,
he did not have Horner syndrome.
Initial Neuroradiologic Findings
Magnetic resonance imaging (MRI) on admission showed
no parenchymal lesions but axial T2-weighted images
demonstrated a large crescent intramural hematoma in
the right internal carotid artery (ICA) and a smaller one
in the left ICA, located at the extracranial-intracranial
transition of both ICAs. Intracranial three-dimensional
time-of-flight (TOF) magnetic resonance angiography
(MRA) suggested a filiform stenosis of the right petrosal
ICA and revealed reduced signal intensities within both
intracranial ICA segments (Figs. B18.1, B18.2).
Suspected Diagnosis
mon carotid arteries (CCAs) (Figs. B18.3, B18.4). Both ICAs
showed reduced flow with peak flow velocities of about
60 cm/s along with increased pulsatility on the right side
with a preserved diastolic flow component (not shown).
The Doppler spectrum of both vertebral arteries (VAs) was
normal.
Transcranial Duplex Sonography
A poststenotic flow pattern was observed in both M1-MCA
as well as both A1-ACA segments. Turbulences and increased flow velocities were seen in both posterior communicating arteries (PCoAs), reaching a peak systolic flow
of 140 cm/s on the left side and 192 cm/s on the right side.
The left distal posterior cerebral artery (PCA) segments
showed normal flow signals. On the right side, flow velocities in the distal PCA segments were increased, indicating
leptomeningealcollateralflow(Figs. B18.5–B18.10). The
ophthalmic arteries (OAs) were not examined.
Conclusion
Bilateral high-grade ICA stenosis of hemodynamic relevance in the distal ICA. A more detailed localization was
notpossibleastheOAswerenotexamined.Collateralization via both PCoAs and leptomeningeal arteries via the
right PCA.
BilateraldistalICAdissection.
Questions to Answer by Ultrasound Techniques
• Were there sonographic signs of dissection?
• Can the presumed right distal ICA stenosis be detected?
• If so, were there collateral pathways?
• Were there any further intracranial stenotic processes?
Initial Neurosonologic Findings
Extracranial Duplex Sonography
B-mode imaging revealed no atherosclerotic vascular
changes and no typical signs of vessel dissection. Doppler
spectrum analysis showed high pulsatility in both com-
Conventional Angiography
Digital subtraction angiography (DSA) was performed to
analyze the cerebral as well as renal arteries. Multiple
irregular concentric constrictions with normal and dilated
intervening segments were found in both distal extracranial ICAs, with a right-sided predominance. These “strings
of beads” were considered typical of fibromuscular dysplasia (FMD). Furthermore, there were mild variations in
the caliber of the left renal artery. No abnormalities were
seen within the intracranial vessels. Blood supply of the
anterior circulation was mainly provided via both ICAs and
PCoAs (Figs. B18.11, B18.12).
Figure B18.13shows a schematic drawing of the extra- and
intracranial brain supplying arteries in this patient.
Final Diagnosis
239
Clinical Course (1)
Spontaneous bilateral ICA dissection in FMD was suspected. Intravenous partial thromboplastin time (PTT)guided heparinization was started and then changed to
oral anticoagulation with phenprocoumon for 6 months.
During this time the patient reported continuous improvement of his symptoms.
Follow-up Neurosonologic Findings (3 Months)
Extracranial Duplex Sonography
Doppler spectrum analysis showed normalized flow signals in both CCAs (Figs. B18.14, B18.15)andICAs.
Transcranial Duplex Sonography
Normal and symmetric flow signals were seen in all detectable intracranial vessels. The previously seen turbulent
flow pattern and raised flow velocity in projection of both
PCoAs had completely subsided (Figs. B18.16–B18.20).
Conclusion
Flow normalization in all detectable vessels indicating
hemodynamic restitution.
Clinical Course (2)
Follow-up after 6 months revealed no further clinical
events. Intracranial TOF MRA showed a mild residual diminution of the signal in the left proximal ICA
(Fig. B18.21). Treatment was changed to antiplatelet therapy with aspirin.
Final Diagnosis
Bilateral spontaneous distal ICA dissection with excellent
restitutioninFMD.
Fig. B18.1 MR T2-weighted image, axial plane. Crescentic intramural hematoma at the extracranial-intracranial transition of both ICAs
(arrows).
Degree of Neurosonologic Difficulty: Medium
Fig. B18.2 3D TOF MRA, axial MIP. Lumen reduction in the petrosal
part of the right ICA (arrowhead). Note the decreased signal in both
carotid siphons caused by poststenotic low flow (arrows).
Fig. B18.3 Extracranial duplex, longitudinal plane. Increased pulsatility in the left CCA (flow velocity: 93/33 cm/s).
Case 18 Bilateral Internal Carotid Artery Dissection
240
Degree of Neurosonologic Difficulty: Medium
Fig. B18.4 Extracranial duplex, longitudinal plane. Increased pulsa-
tility in the right CCA (flow velocity: 122/25 cm/s).
Fig. B18.6 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Poststenotic flow pattern and reduced velocities in
the right M1-MCA (flow velocity: 64/44 cm/s).
Fig. B18.5 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Poststenotic flow pattern and reduced velocities in
the left M1-MCA (flow velocity: 50/32 cm/s).
Fig. B18.7 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Normal flow in the distal left P2-PCA (flow velocity:
38/17 cm/s).
Fig. B18.8 TCCS (transtemporal approach), right-sided insonation,
thalamic plane. Increased flow velocity in the right P3-PCA, indicating leptomeningeal collateral flow (flow velocity: 96/49 cm/s).
Fig. B18.9 TCCS (transtemporal approach), left-sided insonation,
anterior coronal plane. Turbulent and increased flow in the projection of the carotid siphon considered to correspond to a functional
stenosis of the left PCoA (flow velocity: 141/87 cm/s).
Final Diagnosis
241
Degree of Neurosonologic Difficulty: Medium
Fig. B18.10 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Turbulent and increased flow in the right PCoA (flow
velocity: 192/106 cm/s.
Fig. B18.11 DSA, right ICA injection, lateral view. Multiple irregular
concentric constrictions in the right distal ICA suggestive of dissection in fibromuscular dysplasia. Note the extracranial start (thin
arrows) and the extension into the intracranial vertical C6 segment
of the ICA. Also note the signal gap at the ICA transition into the
horizontal C6 segment probably indicating an embolus (thick arrow).
Fig. B18.12 DSA, left VA injection, posteroanterior view. Note the
weak contrast filling of the MCA territories via leptomeningeal PCA
collaterals (arrows).
Fig. B18.13 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 18. Bilateral distal highgrade ICA stenosis (circles). There is collateral blood flow toward the
bilateral anterior circulation via both PCoAs and on the right side also
via leptomeningeal collaterals from the right PCA (green arrow).
Case 18 Bilateral Internal Carotid Artery Dissection
242
Degree of Neurosonologic Difficulty: Medium
Fig. B18.14 Extracranial duplex, longitudinal plane. Normalized left
CCA flow (flow velocity: 99/34 cm/s).
Fig. B18.16 TCCS (transtemporalapproach), right-sidedinsonation,
anterior coronal plane. Normalized flow in the right distal ICA (flow
velocity: 45/19 cm/s).
Fig. B18.15 Extracranial duplex, longitudinal plane. Normalized
right CCA flow (flow velocity: 94/29 cm/s).
Fig. B18.17 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normalized flow signal in the left M1-MCA (flow
velocity: 65/29 cm/s).
Fig. B18.18 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Normalized flow signal in the right MCA (flow velocity: 80/37 cm/s).
Fig. B18.19 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Unchanged normal flow signal in the left P2-PCA
(flow velocity: 48/23 cm/s).
Discussion
243
Degree of Neurosonologic Difficulty: Medium
Fig. B18.20 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Normalized flow signal in the right P2-PCA (flow
velocity: 54/29 cm/s).
Discussion
Clinical Aspects
Here we describe a 45-year-old patient with history of
migraine and spontaneous bilateral ICA dissection in previously unknown fibromuscular dysplasia (FMD). Spontaneous ICA dissections are the most common cause of nonatherosclerotic ischemic strokes in young patients.
Migraine and FMD are considered to be potential risk
factor for a spontaneous dissection. A bilateral ICA dissection is uncommon, and has been observed in 5–28 % of
cases (Gout et al. 1999, Hart and Easton 1983, Zetterling et
al. 2000). Bilateral involvement is more often present in
patients with an underlying connective-tissue disease or
FMD. In patients with bilateral ICA dissection FMD is found
in up to 50 % (Schievink et al. 1994a). In the general population, recurrent dissection is not a major concern in ICA
dissection as its annual risk is approximately 1 % (Schievink and Roiter 2005). In FMD the risk of recurrence seems
to be higher. An analysis in 103 patients over a median
observational period of 4 years demonstrated dissection
recurrenceinfivepatientsofwhomfourhadFMD(deBray
et al. 2007) (for further discussion on spontaneous dissection and role of migraine, see Case 11, p.183, and for further
details about FMD, see Case 13, p. 204).
Angiologic and Anatomic Aspects
Our case of bilateral distal extracranial ÌCA stenoses illustrates the diagnostic difficulties in evaluating the craniocervical transition. Ultrasound is a well-established
method for the evaluation of the extracranial ICA as the
carotid bifurcation and the proximal ICA segments can be
visualized directly. The combination with hemodynamic
parameters permits excellent determination of grades of
stenosis. However, analysis of the distal extracranial ICA,
Fig. B18.21 3D TOF MRA, axial MIP (6 months after onset of symptoms). Almost normalized findings. Note the mild residual reduction
in the signal in the left proximal ICA (arrowhead).
which lies deep to the mandibular ramus, may cause considerable problems. In addition, the ICA often follows an
elongated vessel course. Evaluation has therefore often to
rely on the assessment of indirect hemodynamic parameters. In our case, these were the high pulsatility of the CCA
and proximal ICA with well-preserved diastolic flow,
which indicated distal flow obstruction. Intracranially,
poststenotic flow patterns were observed in the MCA
and ACA and functional stenosis in both PCoAs, which
were serving as collaterals. All factors were indicative of
high-gradeICAstenosesneartheskullbase.Moreprecise
localization of the ICA obstruction was not possible because of the unknown flow pattern in the OA. In view of the
remaining diastolic flow in the proximal vessels, a near
occlusion or occlusion of the ICA below the OA origin was
considered unlikely. Direct imaging of the more distal ICA
can be attempted using the linear transducer in an axial
plane pointing toward the base of the skull, or a 2 MHz
TCCS probe using the same approach, neither of which
were performed in our case. Another technique that can
be used to visualize the distal ICA is the transoral approach,
with a 5–9MHz convex array transducer (Kishikawa et al.
2002, Yasaka et al. 1998). However, this is not used in our
ultrasound laboratory. Both PCoAs in our patient demonstrated an increase in flow velocity and turbulent flow
signals, which could also have been interpreted as bilateral
carotid siphon or C2-ICA stenoses. In limited insonation
conditions sometimes the differentiation between a “real”
stenosis caused by vessel narrowing and a “functional”
stenosis caused by raised flow in a nonstenosed ACoA or
PCoA can be difficult, especially in the latter vessel segment. However, in our case sufficient clinical and radiological information was available that made bilateral carotid siphon stenoses unlikely. First, our patient had no
vascular risk factors and no extracranial atherosclerotic
vessel changes which could have explained further, more
distal ICA stenoses. Second, the intracranial TOF MRA
Case 18 Bilateral Internal Carotid Artery Dissection
244
clearly demonstrated signal reduction in the proximal
intracranial ICA indicative of an ICA pathology clearly inferior to the carotid siphon.
Insonation of the horizontal C6-ICA segment would certainly have been of help, but this was not performed in this
patient. Information about the C6-ICA segment is of particular interest, as C6-ICA stenoses can occur as frequently
as those within the carotid siphon or the terminal ICA
(Boseetal.2007).TheproximalintracranialICAwas
thought to be inaccessible by ultrasound for a long time.
Meanwhile systematic data about insonation of the C5-ICA
segment(Jurgitaetal.2002)aswellasofthehorizontal
part of the C6-ICA segment (Eggers et al. 2007a) have been
presented (for further discussion on C6-ICA segment in-
Degree of Neurosonologic Difficulty: Medium
sonation, see also Chapter 2, “Intracranial Arteries,” p. 24).
Our case illustrates that the combination of several modalities, i. e., ultrasound results, clinical information, and radiologic findings might be necessary to allow a correct
evaluation.
We assume that the dissection was facilitated by the
presence of FMD. The typical “string of beads” pattern
could not be visualized by duplex ultrasound because of
its distal location. As this is often the case, ultrasound has a
low sensitivity compared with other angiologic methods
forthedetectionofFMD(Arning2001)(forfurtherdiscussion on imaging in FMD, see also Case 13, p. 204).
Apart from the bilateral dissection, there was another
peculiarity in our patient: The location of both stenoses
was exceptionally distal. Extracranial ICA dissections usually start 2–3 cm above the carotid bifurcation, extending
distally over a variable length. At the ICA entry into the
carotid canal within the petrous bone, the vessel lumen
usually normalizes (de Bray et al. 2007, Schievink 2001). A
continuation of the dissection into the petrous segments of
the ICA is rare. The literature reports just seven cases in
which a dissection could be seen in the horizontal petrous
part of the ICA. This was, however, restricted to this area
alone (Huang et al. 2007). In our case the dissection started
just below the skull base and extended into the vertical
petrous ICA segment. For further details about DSA, MRI
techniques, and CTA in ICA dissection, see Case 11 (p.183).
Case 19
Vertebral Artery Dissection with Distal Occlusion
245
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
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 magnetic resonance imaging (MRI) showed a
subacute cerebellar ischemic infarction in the right posterior inferior cerebellar artery (PICA) territory (Fig. B19.1).
No sign of intramural hematomawas observed on axial T1and T2-weighted images. Time-of-flight (TOF) magnetic
resonance angiography (MRA) revealed reduced signal intensity in the proximal right V1-VA segment (not shown)
and an absentdistal vertebral artery(VA)signal (Fig. B19.2).
The left VA was normal. A fetal-type posterior cerebral
artery (PCA) was seen on the right side. The basilar artery
(BA) and all other intracranial vessels were unremarkable.
Suspected Diagnosis
Cerebellar ischemia in the right PICA territory caused by
right 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 occlusion?
• Was there evidence of dissection?
Initial Neurosonologic Findings
Extracranial Duplex Sonography
Normal flow signals were found in the carotid arteries. The
left VA was inconspicuous, revealing 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 flow signal with
a low and short systolic flow and completely absent
diastolic flow component in its extracranial segments
(Figs. B19.3–B19.7).
Transcranial Duplex Sonography
Transtemporal insonation revealed normal flow signals in
allintracranialvessels.Transforaminalexaminationdemonstrated normal flow in the BA and the left V4-VA segment. A retrograde flow with reduced velocity was seen in
projection of the right V4-VA segment (Figs. B19.8–
B19.10).
Conclusion
Dissection in the right V2-VA segment with suspected
distal VA occlusion, below the origin of the PICA. Retrograde filling of the right V4-VA segment.
Conventional Angiography
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 fibromuscular dysplasia (FMD). The right VA showed distinct
caliber variations commencing at the entrance of the VA
into the transverse foramen. A filiform stenosis was seen in
the distal V2 segment with complete occlusion in the distal
V3 segment. There were several small vessels originating
from theright V2 segment . The left VA showed an “intimal
flap” in the central aspect of the V2 segment. The BA was
normal. Retrograde flow to the distal part of the right V4VA segment was seen. The remaining intracranial vessels
were normal and there was no evidence of FMD in the
renal arteries (Figs. B19.11–B19.13).