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Case 16 Giant-cell Arteritis with Bilateral Intracranial V4 Vertebral Artery Stenosis
226
atherosclerosis.Thefindingsweremoresuggestiveofarteritis with the STeA insonation demonstrating the dark
halo sign and with the raised CRP. The dose of prednisolone was therefore increased to 30 mg daily.
Follow-up Neurosonologic Findings (6 weeks)
Extracranial Duplex Sonography
The left V2-VA segment showed unchanged normal flow
signals. The right V2-VA segment, however, now demonstrated an even more pronounced high-resistance flow
Degree of Neurosonologic Difficulty: Medium
signal with a small and short systolic flow and completely
absent diastolic flowcomponent (Figs. B16.10, B16.11). No
dark halo sign was seen in either of the STeAs.
Transcranial Duplex Sonography
Flow velocity in the left proximal V4-VA segment now
reached 355/255 cm/s. No flow signal was detected in
projection of the right V4-VA segment. BA identification
again was not possible (Fig. B16.12). Both PCAs further on
presented poststenotic flow patterns.
Conclusion
Secondary occlusion of the right V4-VA segment with
compensatory flow increase in the preexisting left proximal V4-VA stenosis. Alternative diagnosis: Additional progression of the left V4-VA stenosis.
Clinical Course (2)
During the ultrasound examination the patient again developed vertigo and diplopia lasting a few minutes. A CT
angiogram was performed and confirmed the neurosonologic findings of a long-segmented right VA occlusion
starting at the V3-V4 junction and ending before the origin
of the posterior inferior cerebellar artery (PICA). The left
VA stenosis appeared unchanged (Fig. B16.13). Because of
the new ischemic event and the progression of the occlusive disease, the steroid dose was increased to 50 mg
prednisolone daily. The CRP was still slightly elevated
(6.8 mg/L). Based on CRP monitoring the steroid dosage
was gradually reduced over the ensuing months until
below Cushing levels. The 2-year follow-up revealed no
further clinical eventsand showed unchanged neurosonologic findings with low-dose prednisolone (2 mg/day).
Final Diagnosis
Recurrent vertebrobasilar TIAs of hemodynamic origin
caused by bilateral VA stenosis starting at the V3-V4 junction with extension to the proximal V4 segment and secondary occlusion of the right V4-VA below the PICA origin.
Giant cell arteritis seemed to be the most likely etiology .
Fig. B16.1 CTA, coronal MIP. Bilateral severe VA stenoses, right
(arrows) > left (arrow) at the entrance into the dura mater.
Fig. B16.2 Extracranial duplex, longitudinal plane. Mild atherosclerotic vascular changes with small hyperechogenic plaques (maximal
width: 1.7 mm) in the left distal CCA and carotid bifurcation. Note
there are no signs of vasculitis.
Final Diagnosis
227
Degree of Neurosonologic Difficulty: Medium
Fig. B16.3 Extracranial duplex, longitudinal plane. Mild atheroscler-
otic vascular changes with small hyperechogenic plaques in the right
carotid bifurcation (arrows).
Fig. B16.5 Extracranial duplex, longitudinal plane. High resistance
flow signal with reduced flow velocity in the right V2-VA and increased pulsatility (flow velocity: 29/6 cm/s). Diameter: 3.6 mm.
Fig. B16.4 Extracranial duplex, longitudinal plane. Normal flow signal in the left V2-VA (flow velocity: 40/17 cm/s). Diameter: 3.2mm.
Fig. B16.6 Extracranial duplex (linear transducer 11 MHz). A branch
of the right STeA shows reduced color filling and a vessel wall
thickening in form of a dark halo sign (arrows).
Fig. B16.7 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Reduced flow velocity and poststenotic flow pattern
in the left distal P2-PCA (flow velocity: 21/12 cm/s).
Fig. B16.8 TCCS (transforaminal approach). Increased flow velocity
in the left V4-VA suggestive of stenosis (flow velocity: 230/
121 cm/s).
Case 16 Giant-cell Arteritis with Bilateral Intracranial V4 Vertebral Artery Stenosis
228
Degree of Neurosonologic Difficulty: Medium
Fig. B16.9 TCCS (transforaminal approach). Severe turbulence and
raised flow velocity in the right V4-VA hindering a clear flow velocity
measurement.
Fig. B16.11 Extracranial duplex longitudinal plane. Follow-up after
6 weeks: High resistance flowsignal in the right V2-VAreveals a small
and short systolic flow and completely absent diastolic flow component indicative of distal vessel occlusion proximal of the PICA origin
(flow velocity: 19/0 cm/s).
Fig. B16.10 Extracranial duplex, longitudinal plane. Follow-up after
6 weeks: Normal flow in the left V2-VA (flow velocity: 45/23 cm/s).
Fig. B16.12 TCCS (transforaminal approach). Follow-up after 6
weeks: Turbulence and increased flow in the left V4-VA suggestive
of progressive stenosis (flow velocity: 355/249 cm/s).
Discussion
Clinical Aspects
Here we discuss a patient with recurrent TIAs in the posterior circulation. This evaluation was based on the type
and temporal pattern of symptoms lasting for minutes
only. The combination of transient vertigo, diplopia, and
gait disturbances was rather suggestive of impaired brain
stem perfusion of hemodynamic origin. This assumption
was confirmed by the radiologic findings of bilateral VA
stenoses starting at the level of the V3–V4 junction with
extension to the proximal V4 segments.
Three months prior to the reported neurologic symptoms, giant cell arteritis was diagnosed and histologically
confirmed in one temporal artery. Giant cell arteritis is an
autoimmune vasculitis of unknown origin. The disease
almost exclusively occurs in individuals older than 50
years of age. The age-adjusted incidence is 24.2/100 000
for women and 8.2/100 000 for men (Salvarani et al. 1995).
The histopathologic picture is a granulomatous inflammation of the media layer, which usually involves the entire
vessel wall. Fragmentation of the internal elastic lamina is
characteristic. Giant cells are commonly present. In up to
100 % of cases the STeA, the VA, the OA, the posterior ciliary
arteries, or a combination of the above are affected (Wilkinson and Russell 1972). Vessel wall changes might also
be found in other peripheral arteries, such as the occipital
artery,facialartery,subclavianartery,axillaryartery,brachial artery, ulnar artery, radial artery, femoral artery,
popliteal artery, posterior tibial artery, and in the dorsal
pedal arteries (Schmidt et al. 2002a). Intracranial involvement may also occur but is rare. Salvarini and co-workers
found only 9 patients in the literature including their own
2 patients with histologically proven temporal arteritis
that also had intracranial vasculitis shown by angiography
and/or histology (Salvarini et al. 2006). In particular, the
intracranial VAs are seldom affected. The typical predominantly extracranial vascular involvement is in part explained by the affinity of inflammation to the elastic fibers.
As intracranial arteries have less elastic fibers in the media,
lack an external membrane, and have an internal membrane which is rather small, they are seldom involved.
Affliction of the extracranial VA will cease abruptly at least
a few millimeters after perforating the dura mater. If
present, a symmetric involvement of the VA is common
in giant cell arteritis (Crompton 1959, Wilkinson and Russell 1972).
The main clinical symptoms are headaches, visual disturbances, muscle pains, jaw claudication, and fever. Neurologic manifestations may be cranial or peripheral neuropathies, and neuro-otologic and neuropsychiatric syndromes. The spectrum of symptoms in the event of VA
involvement comprises headaches and neck pains but
also TIAs and stroke. A retrospective study reported cerebral ischemia in 7 % of patients with giant cell arteritis, in
whom about one-third occurred in the posterior circulation (Caselli et al. 1988). TIAs in giant cell arteritis are
reported to be 2.5 times more common than in patients
with atherosclerotic vessel wall changes (Lipton et al.
1987).
A definitive diagnosis is made following the criteria of
the American College of Rheumatology which includes,
besides the collection of demographic, clinical, and paraclinical parameters, a biopsy and histologic evaluation of
the STeA (Hunder et al. 1990). The latter is the diagnostic
gold standard. However, as the disease might show only
segmental involvement of the above arteries, a biopsy
result may be negative in 9–44 % of patients with clinical
positive signs of giant cell arteritis (Karassa et al. 2005).
Treatment comprises the immediate prescription of initially high-dose corticosteroids. In addition to a review of
the clinical symptoms, CRP and ESR are suitable parameters for treatment monitoring. In progressive or relapsing
disease immunosuppressive therapy, for example, cyclophosphamide in addition can be considered (Ruegg et al.
2003).
The most frequent cause of occlusive VA disease, however, is atherosclerosis. Intracranial VA atherosclerosis occurs as frequently as in the proximal V0/V1 segments, and
bilateral involvement is also common (Caplan et al. 2004)
(see also Case 8, p. 165). As our patient showed atherosclerotic vascular changes in all brain-supplying arteries,
an atherosclerotic etiology had also to be considered, particularly in view of his age and vascular risk profile. Furthermore,ourpatientdidnothavethepainsthattypically
occur in acute giant cell arteritis. Neck pain is a major
finding in VA arteritis and was present in all eight patients
Discussion
Fig. B16.13 CTA, coronal MIP. Follow-up after 6 weeks: Long-segment occlusion of the right V4-VA beginning at its V3-V4 junction
(thin arrows). Unchanged preexisting left-sided VA stenosis (thick
arrow). Note also the calcified plaque in the distal right V4-VA
(arrowhead).
in the literature so far. Also, in seven of these eight patients, stroke was a clinical feature and mortality was
distinctly higher than in patients with atherosclerosis
(Ruegg et al. 2003).
Arguments in favor of arteritis were the previous histologic confirmation, the sonographic dark halo sign in the
STeA, the location at the dural entrance, and the clinical
stabilization under steroid medication. Even the secondary right VA occlusion, despite the intensified steroid medication, could be compatible with arteritis as a number of
patients with rapidly progressing stenoses despite immunosuppressive therapy have already been reported in the
literature (Ruegg et al. 2003). A final conclusive diagnosis,
however, was not possible in our case.
Angiologic and Anatomic Aspects
Duplex ultrasound can relevantly contribute to the diagnosis of a giant cell arteritis, particularly by visualization of
the inflammatory vessel wall which appears as a hypoechogenic mural thickening, also called dark halo sign
(Pfadenhauer and Weber 2003, Schmidt et al. 1997). A
hypoechogenic vessel wall may also occur in intramural
hematoma, i. e., dissection but is then, in contrast to the
arteritis ofeccentric location. Hypoechogenicity in arteritis
appears mostly concentric (de Bray et al. 1997). In positive
STeA findings this is, however, irrelevant as dissections
hardly ever occur. The mural thickening in giant cell arteritis may also result in stenoses or occlusions of the affected
vessel segments. A single-center study of 751 patients
229
Degree of Neurosonologic Difficulty: Medium
Case 16 Giant-cell Arteritis with Bilateral Intracranial V4
230
revealed an 88 % diagnostic sensitivity for ultrasound in
relation to the clinical diagnosis and a 95 % diagnostic
sensitivity in relation to a positive histologic finding. Considering the clinical diagnosis, a positive dark halo sign had
a specificity of 99.5 % and stenoses or occlusions had a
specificity of 96 % (Schmidt and Gromnica-Ihle 2003). A
metaanalysis of 23 studies comprising a total of 2036
patients, however, demonstrated lower values reflecting
the heterogeneity of investigators and instrument used.
Sensitivity and specificity of the halo sign were 55 % and
94 %, respectively, compared with clinical diagnostic
American College of Rheumatology (ACR) criteria and
69 %and 82 %, respectively, compared with biopsy (Karassa
et al. 2005). Potential pitfalls for ultrasound may be an
Degree of Neurosonologic Difficulty: Medium
atherosclerotic STeA stenosis or false-positive halo signs
that may be present in infectious or malignant diseases
(Karassa et al. 2005). Ultrasound diagnosis in vessels other
than the STeA is more difficult and positive findings less
frequent. For example, in the VA, a positive dark halo sign
was reported in only 2.2 % of cases with known giant cell
arteritis (Pfadenhauer et al. 2005). This low identification
rate is probably caused by the limited B-mode insonation
conditions within the distal V2- and the V3-VA segments,
caused by the vessel course and its close relation to the
spinal column. In this location, alterations of vessel wall
echogenicity are difficult to assess. Correspondingly,in our
patient the typical “dark halo” sign was found only in the
STeA and not in the VA.
More recently, high-resolution MRI has demonstrated
promising results in imaging of giant cell arteritis. In single
cases, a mildly hyperintense signal of the affected vessel
walls has been reported in T2-weighted MRI (Reinhard et
al.2003).BetterresultsareachievedifT1-weightedcontrast MRI is used which allows direct imaging of the mural
thickening and mural enhancement. Positive MRI findings
revealing vessel inflammation were also reported in a
small study of nine patients with clinically diagnosed giant
cell arteritis. In one of these patients, inflammation of the
occipital artery was seen while the STeA was spared (Bley
et al. 2005) In a larger series of 64 consecutive patients a
sensitivity of 80.6% and a specificity of 100% has been
recently reported when compared to clinical criteria including temporal artery biopsy (Bley et al. 2007).
CT and CTA can currently contribute little toward a confirmation of a giant cell arteritis although stenoses or
occlusions, like in our case, can be well assessed (for further discussion on sonographic and radiologic findings in
distal VA stenosis, see also Case 8, p.165).
Ultrasound diagnosis of secondary proximal V4-VA occlusioninourreportedcasewasbasedontheonlysmall
remaining systolic flow and completely missing diastolic
flow component suggestive for an occlusion prior to the
origin of the PICA. However, occlusion may also be present
in cases with a preserved minimal diastolic flow as arterial
collaterals toward the neck muscle or the occipital artery
may exist. The latter underlines that ultrasound, in particular within the posterior circulation, is highly specific but
that its sensitivity is comparatively low (see also Chapter 5,
“Intracranial Pathology,” p. 94).
A special feature of the reported case is the secondary
flow velocity increase in the stenosed left VA and the
concurrent right occlusion. As only flow velocities were
measured, a differentiation between a worsening of stenosis or a flow rise due to an increased collateral flow by
ultrasound was not possible. The only slight increase of
flow velocity in the left V2-VA from 40/17 cm/s to 45/
23 cm/s seemed not sufficient to prove a flow rise as small
differences can also be caused by slightly different angle
correction. However, as CTA in our patient demonstrated
an unchanged left VA stenosis the flow velocity increase
was finally attributed to a raised collateral flow.
Another issue of interest is the exact allocation of VA
segments. The V0-V1 transition is usually not further differentiated. The V1-V2 transition is well defined at the
place where the VA begins its intraforaminal course. The
V2-V3 transition is only rarely of clinical interest. A determination of the V3-V4 border, permitting differentiation
between extra- and intracranial VA, however, is of clinical
interest; for example, an intracranial location of a VA
aneurysm or dissecting aneurysm carries the potential
risk of intracranial hemorrhage and anticoagulation treatment should then be avoided. As in our case, an exact
anatomic localization of VA pathology might also help to
clarify the etiology, as an intracranial localization of vascular pathology is more indicative for atherosclerosis.
Transcranial color-coded sonography is usually not able
to answer the above question. Using the transforaminal
insonation approach, both the V3 and the V4-VA segments
can usually be visualized but the exact differentiation
between intra- and extradural course is usually not possible. In our patient, the stenoses seemed to be located
intracranially in the proximal V4-VA segment, but CTA
suggested that their location was extracranial—at the bor-
der between the extracranial and intracranial parts.
Case 17
Ascending Middle Cerebral Artery Occlusion
231
Clinical Presentation
A 39-year-old human immunodeficiency virus (HIV)-positive man was admitted to the department of infectious
diseases after developing mild speech disturbance and
hypesthesia of his right face. An opportunistic infection
or lymphoma was suspected, but magnetic resonance
imaging (MRI) revealed an ischemic cortical stroke in the
left middle cerebral artery (MCA) territory. An intracranial
MR angiogram (MRA) demonstrated a proximal M2
branch occlusion of the left MCA (Figs. B17.1, B17.2). There
were no known vascular risk factors. His symptoms improved spontaneously and a diagnostic workup was initiated. No heparin or antiplatelet therapy was given. Five
days later his condition acutely worsened, with severe
right-sided hemiparesis and marked aphasia. He was
then transferred to our stroke unit for further evaluation
and treatment (National Institute of Health Stroke Scale
[NIHSS] score 10).
Initial Neuroradiologic Findings
Following transfer to our department, a cerebral MRI revealed a large left-sided infarct in the striatum extending
into the parietal lobe. The intracranial MRA now demonstrated a left proximal M1-MCA occlusion (Figs. B17.3,
B17.4).
Suspected Diagnosis
Initial Neurosonologic Findings (Day 1)
Extracranial Sonography
B-mode sonography revealed a single hyperechogenic
atherosclerotic plaque in the left carotid bifurcation at
theoriginoftheinternalcarotidartery(ICA).Doppler
spectrum analysis showed a flow signal with reduced
flow velocity in the left ICA (flow velocity: 24/8 cm/s).
Flow signals in the right ICA (flow velocity: 58/23 cm/s)
as well as in both external carotid arteries (ECAs) and the
vertebral arteries (VAs) were normal (Figs. B17.5–B17.7).
Transcranial Duplex Sonography
In projection of the left M1-MCA segment within the sylvian fissure no flow signal was detectable. The terminal left
C1-ICA segment showed a flow pattern similar to the extracranial ICA (31/16cm/s). In the left A1-ACA (flow velocity: 147/70cm/s) and proximal P2-PCA (flow velocity: 94/
47 cm/s) segments there was increased nonturbulent flow,
indicating leptomeningeal collateralization. Normal flow
velocities were seen in all the right cerebral arteries and in
both ophthalmic arteries (OAs) (Figs. B17.8–B17.13).
Conclusion
Left proximal M1-MCA occlusion. Leptomeningeal collateral blood flow via the left anterior and posterior cerebral
arteries.
Ischemic reinfarction in the left MCA territory caused by
M1-MCA occlusion.
Questions to Answer by Ultrasound Techniques
• Was there evidence of atherosclerotic change or vasculitis in the extracranial brain-supplying arteries?
• Was there a sustained left M1-MCA occlusion?
• If so, was there evidence of collateral leptomeningeal
blood flow via the anterior (ACA) and/or posterior (PCA)
cerebral arteries?
Conventional Angiography (Day 3)
Digital subtraction angiography (DSA) was performed to
exclude or confirm cerebral vasculitis. Complete occlusion
of the left M1-MCA segment was seen. Smooth borders at
the contrast block were suggestive of thrombotic occlusion. There was distinct leptomeningeal collateralization
via the left anterior and posterior cerebral arteries
(Figs. B17.14–B17.16).
Figure B17.17shows a schematic drawing of the extra- and
intracranial brain supplying arteries of the patient.
Case 17 Ascending Middle Cerebral Artery Occlusion
232
Clinical Course
In view of the recent cerebral infarction, no systemic
thrombolysis could be performed. Considering the underlying immunosuppressive disease, absence of vascular risk
factors (no thrombophilia, no findings predisposing for
cardiac embolism), infective cerebral vasculitis was sus-
Degree of Neurosonologic Difficulty: Medium
pected. However, cerebrospinal fluid (CSF) analysis did not
support this hypothesis, revealing only an intrathecal IgG
synthesis,consistent withthe known HIV infection. A mild
hyperlipidemia was thought to be due to the antiretroviral
therapy, but this was not sufficient for it to be the only
causal factor. Cardial embolism was ruled out as far as
possible. An artery-to-artery embolism from the extracranial left ICA plaque was considered to be a potential
Fig. B17.1 Cerebral MRI, apparent diffusion coefficient (ADC) map,
axial plane. Territorial MC A infarct in the left-sided temporal lobe and
anterior insula 2 days after the initial event (arrowheads).
Fig. B17.3 Cerebral MRI, apparent diffusion coefficient (ADC) map,
axial plane. Acute infarction predominantly in the left striatum 7 days
after the initial event. Note the isointense residual temporal infarct
(arrowhead).
Fig. B17.2 Intracranial contrast-enhanced MRA, axial MIP. Absent
signal in a prominent M2-MCA branch suggestive of left proximal
MCA branch occlusion (arrowhead).
Fig. B17.4 Intracranial 3D TOF MRA, axial MIP. In contrast with the
first MRA, there was a proximal left M1-MCA occlusion (arrowhead).
Note the fetal-type PCA in the contralateral side.
Clinical Course
233
Degree of Neurosonologic Difficulty: Medium
Fig. B17.5 Extracranial duplex, longitudinal plane. B-mode imaging
reveals an echogenic atherosclerotic plaque in the left carotid bifurcation with extension to the proximal ICA (arrows).
Fig. B17.7 Extracranial duplex, longitudinal plane. Normal flow signal in the right ICA (flow velocity: 58/23 cm/s).
Fig. B17.6 Extracranial duplex, longitudinal plane. Markedly reduced flow in the left ICA (flow velocity: 24/8 cm/s).
Fig. B17.8 TCCS (transtemporal approach), left-sided insonation,
upper pontine plane. Left terminal C1-ICA with flow signal, similar
to the extracranial ICA (flow velocity: 31/16 cm/s). Absent signal
within the sheath of the left M1-MCA (arrowheads).
Fig. B17.9 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Normal flow in the right M1-MCA (flow velocity:
116/47 cm/s).
Fig. B17.10 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increasednonturbulent flow in the left A1-ACA (flow
velocity: 147/70 cm/s).
Case 17 Ascending Middle Cerebral Artery Occlusion
234
trigger of the initial vessel occlusion that then led to progressive in-situ thrombosis with an adjacent extension of
the clot. Besides the two-step embolism from the ICA
plaque, primary HIV-related in-situ thrombosis with secondary extension also seemed possible. Secondary stroke
prevention was started with aspirin. The patient was
transferred to an external hospital for rehabilitation.
Over the next weeks his neurologic deficits improved
only marginally. The patient was then lost to follow-up.
Degree of Neurosonologic Difficulty: Medium
Final Diagnosis
Two-step MCA infarction caused by a progressive left MCA
occlusion, presumably due to a growing in-situ thrombosis.
Fig. B17.11 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Normal flow in the right A1-ACA (flow velocity: 102/
46 cm/s).
Fig. B17.13 TCCS (transtemporalapproach), right-sidedinsonation,
midbrain plane. Normal flow in the right distal P2-PCA (flow velocity:
55/27 cm/s).
Fig. B17.12 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased nonturbulent flow in the left proximal P2PCA (94/47 cm/s).
Fig. B17.14 DSA, left ICA injection (early arterial phase), posteroanterior view. Complete occlusion of the left M1-MCA with a smooth
margin, suggestive of thrombotic occlusion (large arrowhead). Note
the distinct leptomeningeal collateralization via the ACA (small arrowheads).
Discussion
235
Degree of Neurosonologic Difficulty: Medium
Fig. B17.16 DSA, left VA injection, posteroanterior view. Note the
prominent leptomeningeal collateralization from the PCA via the
occipitotemporal artery (single arrowhead) and the parietooccipital
artery (arrowheads) toward the MCA territory.
Discussion
Clinical Aspects
Here we report of a young HIV-positive patient with a twostep left MCA infarct caused by stepwise left MCA occlusion of unknown etiology. We suspect that an artery-toartery embolic event, originating from extracranial ICA
atherosclerosis, may have triggered the first ischemic
event and the proximal M2-MCA occlusion. The secondary
clinical worsening and the subsequent finding of a proximal M1-MCA occlusion were thought to be caused by a
progressing in-situ thrombosis.
There is growing evidence that HIV-positive patients are
at higher risk of stroke (Engstrom et al. 1989). In the past,
stroke in HIV patients was frequently associated with opportunistic infections, tumors, or an advanced stage of
immunosuppression (Pinto 1996). The introduction of effective antiretroviral drugs, especially the development of
the newer protease inhibitors, has changed the clinical
picture of the disease. Patients live longer and specific
symptoms as well as concomitant infections can be better
controlled. Therefore, knowledge about the disease is
changing and new hypotheses are continuously being
generated. Currentlyit is difficult to find precise epidemio-
logic data on the combination of HIV and stroke. Autopsy
studieshavereportedtheoccurrenceofischemicaswellas
hemorrhagic stroke in these patients. The reported stroke
prevalence ranges from 6 % to 34 % (Berger et al. 1990,
Connor et al. 2000, Kieburtz et al. 1993, Pinto 1996, Rabinstein 2003). Most of these were clinically silent and only
detected at postmortem. The prevalence of clinically diag-
Fig. B17.17 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 17. There is proximal M1MCA occlusion on the left side (circle), and collateral blood flow
toward the left MCA territory via leptomeningeal collaterals from the
left ACA (blue arrow) and the left PCA (green arrow).
Fig. B17.15 DSA, left ICA injection (late arterial phase), posteroanterior view. Note the leptomeningeal collateralization via the ACA
filling the insular branches of the MCA (arrowheads). Note the right
fetal-type PC A.
nosed strokes ranges from 0.5 % to 5 % (Rabinstein 2003).
Risk profilesand stroke etiologyin HIV patients differ from
other stroke patients. Classic vascular risk factors such as
hypertension, diabetes, or hyperlipidemia are of less importance in HIV patients.