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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Neurosonology and Neuroimaging of Stroke
- •Foreword
- •Foreword
- •Table of Contents
- •Physics of Flow
- •Flow Pattern and Flow Velocity
- •Ultrasound Principles
- •Doppler Effect
- •Doppler Shift and Flow Velocity
- •List of Abbreviations
- •Introduction
- •Part A Principles and Rules
- •1 Flow and Ultrasound Basics
- •Flow Dynamics
- •Ultrasound Systems
- •Ultrasound Transducer
- •Imaging Modalities, Parameters, and Settings
- •2 Vascular Anatomy and Structure of Ultrasound Examination
- •General Arterial Anatomy
- •Extracranial Arterial Anatomy
- •Intracranial Arterial Anatomy
- •General Structure of Arterial Ultrasound Examination
- •Special Arterial Anatomy and Ultrasound Anatomy
- •Extracranial Arteries
- •Intracranial Arteries
- •General Venous Anatomy
- •Intracranial Venous Anatomy
- •Extracranial Venous Anatomy
- •General Structure of Venous Ultrasound Examination
- •Special Venous Anatomy and Ultrasound Anatomy
- •Intracranial Veins and Sinuses
- •Extracranial Veins
- •3 Intracranial Hemodynamics and Functional Tests
- •Autoregulation
- •Testing of Autoregulation
- •Neurovascular Coupling
- •Testing of Neurovascular Coupling
- •Metabolic Coupling
- •Other Tests to Assess Differences Between the Right and Left Sides as Markers of Impaired Collateral Function
- •Parameters of Cerebral Hemodynamics
- •Cerebral Blood Flow Velocity
- •Resistance Indices
- •Cerebral Blood Flow
- •Cerebral Circulation Time
- •Cerebral Blood Volume
- •4 Pathogenesis of Stroke
- •Arterial Ischemia
- •Classification of Arterial Stroke
- •Microembolic Signals
- •Spontaneous Microemboli
- •Detection of Microemboli in Patent Foramen Ovale
- •Venous Ischemia
- •5 Vascular Pathology
- •Vessel Wall Pathology
- •Elongations
- •Intima-media Thickness
- •Atherosclerotic Plaques
- •Dissection
- •Fibromuscular Dysplasia
- •Vasculitis
- •Stenoses and Occlusions
- •Ultrasound Criteria of Stenoses
- •Ultrasound Criteria of Occlusions
- •Extracranial Pathology
- •Extracranial Anterior Circulation
- •Extracranial Posterior Circulation
- •Intracranial Pathology
- •Intracranial Anterior Circulation
- •Intracranial Posterior Circulation
- •Collateral Pathways
- •Intracranial Collateral Pathways
- •Intracranial Collateral Pathways in ICA Occlusive Processes
- •Intracranial Collateral Pathways in VA Occlusive Processes
- •Extracranial Collateral Pathways
- •Clinical Relevance of Collateral Pathways
- •6 Angiographic Techniques in Neuroradiology
- •Digital Subtraction Angiography
- •Historical Development
- •Technical Aspects
- •Strengths and Disadvantages
- •Magnetic Resonance Angiography
- •Historical Development
- •Technical Aspects
- •Strengths and Disadvantages
- •Computed Tomographic Angiography
- •Historical Development
- •Technical Aspects
- •Strengths and Disadvantages
- •Current Algorithm at the Charité University Hospital
- •Stroke
- •Intracranial Aneurysm
- •Vasculitis
- •Cerebral Venous Thrombosis
- •Peri-therapeutic Imaging
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Question to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Clinical Course
- •Neurosonologic Findings (Day 20)
- •Final Diagnosis
- •Discussion
- •Part B: Case Histories
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Conventional Angiography (Day 2)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 2)
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Clinical Course (1)
- •Question to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Cerebral CT
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Clinical Course (1)
- •Question to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 42)
- •Neuroradiologic Findings
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Conventional Angiography (Day 2)
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Clinical Course (1)
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Clinical Course (2)
- •Follow-up Neurosonologic Findings (1 Hour)
- •Clinical Course (3)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Clinical Course (1)
- •Questions to Answer by Ultrasound Techniques
- •Follow-up Neurosonologic Findings (Day 2)
- •Clinical Course (2)
- •Follow-up Neurosonologic Findings (Day 7)
- •Clinical Course (3)
- •Follow-up Neurosonologic Findings (6 Months)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Question to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Clinical Course (1)
- •Conventional Angiography (Day 5)
- •Clinical Course (2)
- •Follow-up Neurosonologic Findings (5 Years)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course (1)
- •Follow-up Neurosonologic Findings (2Months)
- •Clinical Course (2)
- •Follow-up Neurosonologic Findings (5Months)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Clinical Course (1)
- •Follow-up Neurosonologic Findings (6 weeks)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Conventional Angiography (Day 3)
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course (1)
- •Follow-up Neurosonologic Findings (3 Months)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Evaluation of Collateral Function
- •Conventional Angiography
- •Clinical Course (1)
- •Follow-up Neurosonologic Findings (Day 20)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Clinical Course (1)
- •Follow-up Neuroradiologic Findings (Day 3)
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 3)
- •Conventional Angiography (Day 4)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Clinical Course (1)
- •Questions to Answer by Ultrasound Techniques
- •Neurosonologic Findings (Day 10)
- •Neuroradiologic Findings (Day 11)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course (1)
- •Question to Answer by Ultrasound Techniques (6 Months)
- •Neurosonologic Findings (6 Months)
- •Clinical Course (2)
- •Questions to Answer by Ultrasound Techniques (8 Months)
- •Neurosonologic Findings (8 Months)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Clinical Course (1)
- •MRI and MR Angiography (10:00 Hours)
- •Questions to Answer by Ultrasound Techniques
- •Neurosonologic Findings (12:00 Hours)
- •Conventional Angiography (16:00 Hours)
- •Clinical Course (2)
- •Questions to Answer by Ultrasound Techniques
- •Follow-up Neurosonologic Findings (6 Months)
- •Clinical Course (3)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 2)
- •Conventional Angiography (Day 4)
- •Clinical Course (1)
- •Clinical Course (2) and Follow-up Neuroradiologic Findings
- •Follow-up Neurosonologic Findings (10 Months)
- •Clinical Course (3)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Conventional Angiography
- •Clinical Course (1)
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings
- •Conventional Angiography
- •Clinical Course
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •Conventional Angiography (Day 2)
- •Clinical Course (1)
- •Follow-up Neurosonologic Findings (4 Weeks)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 1)
- •CT Angiography (CTA) (Day 1)
- •Clinical Course (1)
- •Question to Answer by Ultrasound Techniques
- •Follow-up Neurosonologic Findings (Day 90)
- •Question to Answer by Ultrasound Techniques
- •Follow-up Neurosonologic Findings (Day 180)
- •Clinical Course (2)
- •Final Diagnosis
- •Discussion
- •Clinical Presentation
- •Initial Neuroradiologic Findings (Day 1)
- •Suspected Diagnosis
- •Questions to Answer by Ultrasound Techniques
- •Initial Neurosonologic Findings (Day 20)
- •Conventional Angiography (Day 22)
- •Clinical Course (1)
- •Questions to Answer by Ultrasound Techniques
- •Follow-up Neurosonologic Findings (Day 29)
- •Follow-up Neurosonologic Findings (3 Months)
- •Final Diagnosis
- •Discussion
- •References
- •Index

Case 23 Takayasu Arteritis with Subclavian Artery and Vertebral Artery Stenoses
286
1994, Grosset et al. 1992). In our patient, however, even
this type of collateral flow was not possible because of
bilaterallackoffunctionalPCoAs, a variation of the circle
of Willis which is present in about 16 % of the population
(Hoksbergen et al. 2000b). The coexistence of bilateral
nonfunctional PCoAs and bilaterally impaired VA flow explains the distinctly poststenotic altered flow pattern in
both PCAs, which hardly demonstrated any arterial pulsa-
Degree of Neurosonologic Difficulty: High
tility. It also explains why both PCAs appeared extremely
small on DSA, which could havebeen interpreted as part of
the arteritis even though involvement of the intracranial
arteries is extremelyrare in Takayasu arteritis (Nasu1975).
Aftersuccessfulbypasssurgery,bothPCAflowprofiles
normalized, arguing against the hypothesis of an additional vasculitic PCA involvement.

Case 24
Dissection of the Extracranial Internal Carotid Artery and
Contralateral M1 Middle Cerebral Artery Stenosis
Clinical Presentation
Clinical Course (1)
A 34-year-old woman presented with a 1-year history of
severe headaches that were thought to be caused by repeated hypertensive episodes. She also reported a single
episode of left-sided facialpain and ipsilateral conjunctival
injection lasting for several hours approximately 1 year
ago. After the initiation of antihypertensive treatment the
headaches subsided. However, ambulatory examination of
the optic fundi revealed retinal vessel narrowing. This
finding prompted an ultrasound examination of the
brain-supplying arteries. Transcranial Doppler (TCD) revealed a left M1 middle cerebral artery (MCA) stenosis. In
addition to having hypertension, the patient was a smoker
and used an oral contraceptive. An ambulatory cerebral
computed tomography (CT) scan had been unremarkable.
She was now admitted to our department for elective
catheter angiography to search for extended intracranial
vascular pathology.
Initial Neuroradiologic Findings
Two weeks later, the patient was readmitted to our hospital for further evaluation. On admission she reported a
right-sided neck pain during the catheter angiography
that had been performed 2 weeks ago and a sore throat
on the day following it. The neurologic examination was
normal; in particular, she did not have Horner syndrome.
MRI and MR Angiography (10:00 Hours)
No parenchymal lesions were seen on magnetic resonance
imaging (MRI). On conventional T2-weighted axial MRI
images, a distinctly reduced flow void could be seen in
the distal ICA on axial and coronal images. TOF MRA of the
circle of Willis (CW) demonstrated the known left highgrade M1-MCA stenosis. A reduced signal was observed
within the right terminal ICA. Cervical MRI and MRA of the
extracranial vessels were not performed (Figs.B24.5–
B24.7).
287
Digital subtraction angiography (DSA) demonstrated mild
bilateral extracranial internal carotid artery (ICA) elongations and wide carotid sinuses, but there was no evidence
of stenosis or atherosclerosis. Intracranially a left longsegmented high-grade stenosis of the proximal M1-MCA
segment could be confirmed. Distal to the stenosis, the
residual M1 segment was mildly dilated. Also, a delayed
contrast filling of the distal MCA segments in relation to
the distal ACA segments was seen indicating a high-grade
stenosis of hemodynamic relevance. There were no signs
of vasculitis (Figs. B24.1–B24.4).
Suspected Diagnosis
Asymptomatic left high-grade M1-MCA stenosis. In the
absence of atherosclerotic vessel changes, and the presence of a history of left-sided facial pain with associated
conjunctival injection and headache 1 year previously, an
MCA dissection was suspected.
Questions to Answer by Ultrasound Techniques
• To confirm the left-sided MCA stenosis.
• To search for evidence of other vascular pathology, e. g.,
dissection of the right ICA.
Neurosonologic Findings (12:00 Hours)
Extracranial Duplex Sonography
Therewerenoatheroscleroticvascularchanges.Theright
ICA revealed a long-segmented lumen reduction that
started 2 cm above the carotid bifurcation and continued
over the whole visible distal vessel segment. There were
no typical signs of a dissection. Flow velocity in the right
ICA reached a systolic maximum of 200 cm/s. The right
common carotid artery (CCA) showed a high-resistance
flow signal with a reduced diastolic flow component. The
left ICA, both external carotid arteries (ECAs), and the
vertebral arteries (VAs) presented normal flow signals
(not shown).

Case 24 Dissection of the Extracranial Internal Carotid Arter y and Contralateral M1 Middle Cerebral Arter y Stenosis
288
Transcranial Duplex Sonography
Within the left M1-MCA, transcranial color-coded sonography (TCCS) detected a turbulent stenotic flow (flow velocity: 383/267 cm/s). A poststenotic flow pattern was observed in the left M2-MCA branches. The flow signal of the
right M1-MCA segment appeared normal. The right A1ACA segment showed reversed flow while the left-sided
A1-ACA segment demonstrated increased flow velocities
without turbulence (flow velocity: 225/140 cm/s). Assessment of the posterior cerebral arteries, VAs, the basilar
artery (BA) as well as the ophthalmic arteries (OAs) revealed overall normal orthograde flow signals without
Degree of Neurosonologic Difficulty: High
signs of leptomeningeal or ophthalmic collateral support.
TherewasapositiveoscillationeffectintherightM1-MCA
segment with mild submandibular oscillation of the left
ICAandthedominantleftVAattheatlasloop.Thisindicated collateral flow through the anterior communicating
artery (ACoA) and right posterior communicating artery
(PCoA) (Figs. B24.8–B24.14).
Conclusion
Hemodynamically relevant left high-grade M1-MCA
stenosis. High-grade stenosis of the right extracranial ICA
of hemodynamic relevance, suspicious of dissection, induced by the diagnostic DSA 2weeks previously. Collateral
flow to the right MCA and ACA via the ACoA as well as the
right PCoA.
was assumed to be most likely. After 6 months the patient
was re-examined to evaluate the requirement for longterm secondary stroke prevention.
Questions to Answer by Ultrasound Techniques
• Was there any regression of the right extracranial ICA
stenosis under continuous anticoagulation with phenprocoumon?
• Were there changes in the left M1-MCA stenosis?
Follow-up Neurosonologic Findings (6 Months)
Extracranial Duplex Sonography
No flow signal was observed in the right proximal ICA. The
ipsilateral CCA revealed an increased pulsatility. The right
ECA was normal revealing no indirect signs of collateral
support (Figs. B24.18–B24.21). The left-sided carotid arteries and the VAs were unremarkable.
Transcranial Duplex Sonography
Intracranially the flow pattern was unchanged in relation
to the examination 6 months previously.
Conventional Angiography (16:00 Hours)
DSA performed on the same day demonstrated a conical
lumen reduction of the right ICA directly above the carotid
bifurcation with a filiform stenosis up to the base of the
skull which was suggestive of ICA dissection. CollateralizationviatheACoAwasdirectedtowardtherightMCAand
ACA territory via the left ICA. The right PCoA flowed anteriorly toward the MCA. There was no evidence of leptomeningeal or ophthalmic collaterals. The known high-grade
M1-MCA stenosis remained unchanged (Figs. B24.15–
B24.17). In addition, renal angiography was performed,
which excluded signs of fibromuscular dysplasia.
Clinical Course (2)
The dissection of the right ICA was considered to be of
iatrogenic origin caused by the catheter during the initial
DSA. Intravenous heparin treatment was started, aiming
for a twofold rise in partial thromboplastin time. The patient was then switched to oral anticoagulation with phenprocoumon for 6 months. The etiology of the left M1-MCA
stenosis remained unclear. After exclusion of all other
differential diagnoses, particularly vasculitis, a dissection
Conclusion
Unchanged high-grade stenosis of the left MCA. Secondary
occlusion of the right extracranial proximal ICA with unchanged collateral blood flow via the ACoA and ipsilateral
PCoA.
Conventional Angiography
A third angiography confirmed the occlusion of the right
ICA with a smooth margin (Fig. B24.22).
Figure B24.23 shows a schematicdrawing of the extra- and
intracranial brain-supplying arteries in this patient.
Clinical Course (3)
Secondary stroke prevention was changed to antiplatelet
therapy. During 4 years of follow-up no cerebral ischemia
occurred and no changes in vascular pathology were observed.

Clinical Course (3)
289
Degree of Neurosonologic Difficulty: High
Fig. B24.1 DSA, left ICA injection, left anterior oblique (LAO) pro-
jection. Mild elongation of the ICA and wide carotid sinus without
evidence of atherosclerosis.
Fig. B24.3 DSA, left ICA injection, posteroanterior view. Long-segmented high-grade stenosis of the proximal left M1-MCA (arrow).
Note the dilation of the MCA distal of the stenosis. Also note the
delayed filling of the distal MCA segments in comparison to distal
ACA segments.
Fig. B24.2 DSA, right ICA injection, right anterior oblique (RAO)
projection. Identical mild elongation of the ICA and wide carotid
sinus without evidence of atherosclerosis.
Fig. B24.4 DSA, left ICA injection, posteroanterior view. Magnified
view of Figure B24.3 demonstrating a filiform MCA stenosis (arrows)
and poststenotic vessel dilation.

Case 24 Dissection of the Extracranial Internal Carotid Arter y and Contralateral M1 Middle Cerebral Arter y Stenosis
290
Degree of Neurosonologic Difficulty: High
Fig. B24.5 MRI T2-weighted image, axial plane. Regular findings
without evidence of parenchymal lesions. Note, that the prominent
right PCoA is already visible (arrow).
Fig. B24.7 3D TOF MRA, axial MIP. Reduced signal in the left M1MCA (single arrow), indicating high-grade stenosis. Note that the
right-sided distinct PCoA is not visualized. Note also a reduced signal
in the intracranial right ICA (arrows).
Fig. B24.6 MR T2-weighted image, axial plane. Attenuated flow
void in the right ICA (arrow) indicating a significantly reduced blood
flow.
Fig. B24.8 TCCS, transtemporal approach, midbrain plane. Increased flow velocity in the left M1-MCA indicating high-grade
stenosis (flow velocity: 383/267 cm/s).

Clinical Course (3)
291
Degree of Neurosonologic Difficulty: High
Fig. B24.9 TCCS, transtemporal approach, midbrain plane. Normal
flow pattern in theright M1-MCA (flow velocity: 97/52cm/s) despite
the proximal extracranial high-grade ICA stenosis. Note the limited
quality of the right temporal bone window.
Fig. B24.11 TCCS, transtemporal approach, midbrain plane, left-
sided insonation. Positive oscillation effect on the right M1-MCA
(arrows) caused by oscillation of the dominant left VA, indicating
collateralization via the PCoA. Note also the prominent blue-coded
right PCoA (arrow).
Fig. B24.10 TCCS, transtemporal approach, midbrain plane, left-
sided insonation. Positive oscillation effect on the right M1-MCA
(arrows) caused by mild oscillation of the left extracranial ICA,
indicating cross-flow via the ACoA.
Fig. B24.12 TCCS, transtemporal approach, midbrain plane, leftsided insonation. Increased flow velocity in the left A1-ACA without
turbulence, suggesting collateralization of the contralateral anterior
circulation via the ACoA but also for the ipsilateral MCA territory
(flow velocity: 225/140 cm/s).
Fig. B24.13 TCCS, transtemporal approach, midbrain plane, rightsidedinsonation.TherightA1-ACApresentedwithreversedflow
direction (flow velocity: 192/116 cm/s).
Fig. B24.14 TCCS, transtemporal approach, midbrain plane, leftsided insonation. Turbulent flow and increased flow velocity within
the ACoA (functional stenosis) causedby intracranialcross-flow from
the left ICA.

Case 24 Dissection of the Extracranial Internal Carotid Arter y and Contralateral M1 Middle Cerebral Arter y Stenosis
292
Degree of Neurosonologic Difficulty: High
Fig. B24.15 DSA, right ICA injection, lateral view. Conical lumen
reduction of the right ICA directly above the carotid bifurcation
with a long-segmented filiform stenosis up to the base of the skull
(arrows).
Fig. B24.16 DSA, left ICA injection, posteroanterior view. Collateral
blood flow into the right MCA and ACA via ACoA and retrograde right
A1-ACA. Symmetric filling of both MCAs without delay between the
right and left sides indicating well developed cross-flow (arrowheads). Also note the known long-segmental left M1-MCA stenosis
(arrow).
Fig. B24.17 DSA, left VA injection, posteroanterior view. Collateral
blood flow via the prominent PCoA (arrow) solely into the right MCA.
Fig. B24.18 Extracranial duplex, longitudinal plane. Normal flow in
the left CCA (flow velocity: 122/49 cm/s).

Clinical Course (3)
293
Degree of Neurosonologic Difficulty: High
Fig. B24.19 Extracranial duplex, longitudinal plane. High-resistance
flow signal in the right CCA demonstrating increased pulsatility, i. e.,
a reduced diastolic flow component (flow velocity: 127/ 22 cm/s).
Fig. B24.21 Extracranial duplex, longitudinal plane. Absent flow
signal in the right ICA.
Fig. B24.20 Extracranial duplex, longitudinal plane. Normal flow in
the left ICA (flow velocity: 65/30 cm/s).
Fig. B24.22 Follow-up DSA, right ICA injection, lateral views. Initial
DSA: Normalright ICA (A). Two weeks later: High-grade ICA stenosis
due to dissection (B). Af ter 6 months: Complete ICA occlusion with a
rounded margin resembling occlusion in atherosclerosis (C).
Fig. B24.23 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 24. Right proximal ICA
occlusion (large circle). Left M1-MCA stenosis (small circle). Collateralization of the right MCA territory from the left ICA via ACoA and
retrograde A1-ACA as well as from the PCA via the right PCoA.
Collateralization of the left MCA territory via leptomeningeal collaterals from the lef t ACA.

Case 24 Dissection of the Extracranial Internal Carotid Arter y and Contralateral M1 Middle Cerebral Arter y Stenosis
294
coincidence and the subsequently discovery of typical an-
Final Diagnosis
Asymptomatic high-grade left M1-MCA stenosis caused by
dissection ofunknown etiology. Iatrogenicdissection ofthe
right extracranialICA caused by catheter angiography with
initial high-grade stenosis and secondary ICA occlusion.
Discussion
Clinical Aspects
Here we report of a 34-year-old woman with a suspected
Degree of Neurosonologic Difficulty: High
left intracranial MCA dissection and an iatrogenic dissection of the right ICA.
Dissections are an important cause of stroke, especially
in young patients. Most dissections, however, occur within
the extracranial brain-supplying arteries. In these cases,
diagnosis is mainly made by MRI visualization of the intramural hematoma. Other supporting indicators are the
typical angiographic morphology, missing atherosclerotic
vessel wall changes, and the presence of an intima flap or a
false lumen, in combination with a corresponding clinical
picture (for further discussion on extracranial dissection,
see Case 11, p.183).
Diagnosis of intracranial dissections is more difficult.
Often it is based on an angiographically diagnosed intracranial stenosis in a young patient suffering from a stroke
accompanied by pain. In cases of a concomitant intracranial aneurysm or recent subarachnoid haemorrhage (SAH)
the diagnosis becomes even more likely. However, in the
group of patients aged over 40 a reliable diagnosis becomes more difficult as atherosclerosis might be seen as
a confounding factor and as headaches might also occur in
“normal”-type stroke. With regard to isolated MCA dissections only 23 patients have been reported (Lin et al. 2005),
of which 88% had cerebral infarction and 12 % had SAH. All
the infarctions wereterritorial and none within the border
zones, so that embolic events and not hemodynamic
causes are thought to be the underlying mechanism (for
further discussion on intracranial dissection, see also Case
21, p. 261.
In our case a MCA dissection was considered to be the
most likely cause. In favor of this hypothesis were the
reported left-sided facial pains and headaches, the young
age of the patient, and the absence of atherosclerotic vessel wall changes. The angiographic finding of an irregular
segmental long-segmental stenosis was also compatible
with the hypothesis. However, no ischemia occurred and,
unusual for dissection, the stenosis remained unchanged
over the following years.
During catheter angiography for etiological clarification
of the MCA stenosis our patient experienced an extracranial ICA dissection with initial high-grade ICA stenosis and
subsequent ICA occlusion. Clinically this corresponded to
neck pains which the patient had experienced during and
shortly after thefirst angiography. Because of the temporal
giologic ICA alterations, an iatrogenic cause seemed obvious. Although rarely reported, the question was raised
whether our patient had a particular predisposition to
develop adissection during selective catheter angiography
because of the already present intracranial spontaneous
dissection. An inherited or acquired abnormality of the
intimalormedialvessellayersoroftheelasticconnective
tissue, as for instance in Marfan syndrome, Ehlers–Danlos
syndrome, and pseudoxanthoma elasticum, could result in
increased spontaneous vessel wall vulnerability (Schievink 2001) and possibly also an increased vulnerability,
for example, to mechanical manipulations. Brandt and
coworkers (1988) reported ultrastructural collagen alterations and alterations of the extracellular matrix in skin
specimens of patients with extracranial dissections, which
then may lead to generalized arteriopathy, associated intracranial pseudoaneurysms, an aortic dilatation, and/or
hyper-distensibility of arterial walls (Guillon et al. 2000,
Hausser et al. 2004). However, none of these conditions
were found in our patient, and she had no suggestive
family history. Therefore, the assumption of a particular
predisposition to vessel wall injuries in our patient remains speculative.
Due to the recent advances in noninvasive vascular diagnostics of the brain-supplying arteries, angiography has
lost its importance. However, it has, without doubt, a place
in special indications such as the diagnosis of vascular
malformations, vasculitis, or in any case where endovascular treatment is a potential therapeutic option. But its
use has always been open to criticism because of the
potential side effects. Although the applied techniques
are constantly being improved by using smaller catheters,
hydrophilic guidewires, and digital imaging systems, angiography-related neurologic complications still occur.
Complication rates are usually reported asincidents occurring within 24 hours postintervention (so our case would
not have been included).
A prospective analysis in 2899 angiographic interventions revealed a combined rate of transient and reversible
neurologic deficits of 1.3%. In 14 of these patients (0.5 %),
persisting neurologic deficits occurred (Willinsky et al.
2003). In an older reportincluding eight prospective studies the general neurologic complication rate was 4.1 % and
the rate of persisting neurologic deficits was 1 % (Hankey et
al. 1990). Complication rates are influenced by patient as
well as procedure-related factors. A significantly higher
complication rate has been observed in patients aged 55
years or older (1.8% vs. 0.9 %) (Willinsky et al. 2003). Other
authors,whohavereportednoneurologiccomplications
in those < 50 years or those < 30 years of age, support this
finding (Dion et al. 1987, Heiserman et al. 1994). Other
factors are the angiography duration, the number of vessels catheterized, the experience of the investigator, and
the studied vascular pathology. Thus, a four-vessel angiography is not a routine procedure and vessel intubation has
to be justified on the basis of the very clinical question. If a

Discussion
295
patient with anterior circulation pathology had a dissection during VA intubation, the neuroradiologist would be
at risk of being sued for malpractice. Mani and Eisenberg
(1978) reported an overall complication rate of 3.9 % in a
teaching hospital, compared with 0.9 % in a non-teaching
hospital. When patients with and without occlusive artery
diseasewerecompared,thecomplicationratesinateaching hospital were 4.3 % and 1.2 %, and in a non-teaching
hospital they were 2.6 % and 0.5 %, respectively (Mani et al.
1978). The above finding corresponds well with the fact
that the rate of complications is higher instroke patients in
general than in those with other vascular pathology. A
metaanalysis that compared stroke patients and patients
with intracranial malformations, aneurysms, or vasospasm found a complication rate of 35 % in the former
and 0.8 % in the latter group (Cloft et al. 1999).
In addition to manifest neurologic deficits, angiography
may also cause asymptomatic injuries to the brain. Bendszus and coworkers (1999) analyzed 91 patients who
underwent a total of 100 mostly diagnostic angiographies.
MRI including diffusion-weighted images before and after
angiography revealed 42 postinterventional new lesions
in 23 patients, mostly of embolic appearance. Fortunately,
none of these patients demonstrated aclinically detectable
neurologic deficit. Patients with vascular risk factors and
known vasculopathy were at higher risk of developing
lesions than those without vascular pathology (44 % vs.
13%). The lesion size was small in the majority of cases
but seven of them exceeded 10mm (Bendszus et al. 1999).
This study illustrates that angiography-related embolic
events are frequent but are not sufficiently reflected by
the reported clinical complication rates. Considering the
distribution pattern of the observed cerebral lesions, a
thromboembolic event originating from the catheter itself
or from mechanically dislocated atherosclerotic plaque
fragments seems to be the most likely mechanism.
Side effects related to the contrast agents used and, as in
our case, a dissection of the studied vessel occur less
frequently. A retrospective analysis of 2437 diagnostic
angiographies and 675 neurointerventional procedures
reported 12 dissections (0.4 %). Nine of these were in the
VA, one in the CCA, and two in the ICA (Cloft et al. 2000).
Seven of these patients reported symptoms during contrast injection. In the remaining five the dissection occurred during catheter manipulation. Except for one patient who developed aclinically silent territorialinfarction
all the others had a benign clinical course.
Because of the symptom onset during angiography in
our patient the diagnosis of a carotid dissection was beyond doubt. Interestingly, the patient did not mention her
symptoms at the time of investigation—which was ambulatory. It was therefore missed and only noted when she
was readmitted for further diagnostics and ultrasound
depicted the new vessel pathology. This clinical pattern
indicates that a number of dissections, and also those of
spontaneous nature, might occur silently, leaving a potentially high number of unreported cases.
Angiologic and Anatomic Aspects
The primary ultrasound analysis yielded a long-segmented ICA narrowing with local systolic flow velocities
of up to 200 cm/s but no typical direct signs of dissection.
Typically a more distally located conical-shaped stenosis
or occlusion can be found. Even if the stenosis itself is not
visible, a high-resistance flow signal might indicate the
relevant distal flow obstruction. The latter constellation
alone, however, is not sufficient to diagnose dissection, as
distal stenosis caused by fibromuscular dysplasia (FMD) or
a distal vessel kinking might also result in similar findings.
If atherosclerotic vessel wall changes are completely absent, a dissection, however, becomes more likely. Whenever the patient shows additional head or facial pain and/
or had Horner syndrome the presence of a dissection is
practically evident.
On the contrary, normal ultrasound findings do not exclude a dissection as a distal vessel narrowing less than 70
to 80 % will not result in relevant proximal blood flow
alterations and distal dissecting aneurysms might dominate the morphologic picture. However, in our experience,
if patients are symptomatic, a distal hemodynamically
relevant stenosis is a frequent finding. In patients without
ischemia, extracranial ultrasound examination is normal
in approximately 29 % of cases. In those with ischemia,
normal ultrasound findings occur in 5 % only (Baumgartner et al. 2001). An analysis of purely hemodynamic ultrasound criteriain patients withcerebral ischemia caused by
a dissection found a sensitivity, specificity, and positive
and negative predictive values of 96 %, 92 %, 94 %, and
97 %, respectively (Benninger et al. 2006). Hence, ultrasound is especially useful as a screening tool in patients
with stroke. Further neuroradiologic examination will be
needed for confirmation of diagnosis in equivocal cases
(for further discussion on ultrasound findings in extracranial ICA dissection, see also Case 11, p.183).
During oral anticoagulation, our patient developed a
secondary ICA occlusion which, in contrast with the patient in Case 11, did not result in an additional intracranial
hemodynamic compromise (for further discussion on secondaryvesselocclusion,seealsoCase11,p.183).DSA
demonstrated the hemodynamic effect of the MCA stenosisbyadelayedMCAvesselfillingwhencomparedwith
the ACA contrast filling pattern. Similar to DSA, ultrasound
is also able to reveal flow alterations induced by hemodynamically relevant stenoses. The ultrasound correlate of
the delayed vessel filling is the presence of a poststenotic
flow pattern which was observed in an M2 branch of our
patient. Whenever a poststenotic flow pattern is detected,
astenosisofatleast80%canbeassumed.However,detailed grading, such as in extracranial ICA stenosis, is currently not possible (for further discussion on grading of
intracranial stenoses, see Chapter 5, “Stenoses and Occlu-
sions,” p. 81).
Another interesting hemodynamic aspect was revealed
by DSA. On selective VA filling, the PCoA on the side of the
Degree of Neurosonologic Difficulty: High
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