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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
Case 20 Internal Carotid Artery Dissection with Fast Recanalization
256
Degree of Neurosonologic Difficulty: Medium
Fig. B20.16 DSA, right CCA injection (early arterial phase), lateral
view. Suspected proximal ICA occlusion with a large stump (arrow).
Fig. B20.17 DSA, right CCA injection (late arterial phase), lateral
view. Filling of an irregularly shaped ICA starting at the mid-carotid
region (arrows). The distal ending of the stenosis reaches the vertical
part of the petrous ICA (arrow).
Fig. B20.18 DSA, right CCA injection (late arterial phase), posteroanterior view. Delayed MCA contrast filling on the right side (arrows).
Fig. B20.19 DSA, left ICA injection (early arterial phase), posteroanterior view. Cross-flow from the left ICA to the right MCA. Note
the delayed MCA territory filling of the right MCA (proximal M2
segment) compared with the left MCA (opercular M3 segment).
Final Diagnosis
257
Degree of Neurosonologic Difficulty: Medium
Fig. B20.20 DSA, left ICA injection (capillary phase), posteroante-
rior view. More obviously delayed right-sided circulation in the
capillary phase. Note the parenchymal phase on the left hemisphere
but only insular MCA branch filling on the right side (arrowheads).
Fig. B20.21 DSA, right VA injection, posteroanterior view. Note the
contrast filling of right insular MCA branches (arrows) via a small P1PCA (arrowhead).
Fig. B20.22 Schematic drawing of the extra- and intracranial brain
supplying arteries of the patient in Case 20. High-grade right distal
ICA stenosis (circle). There is collateral blood flow toward the right
MCA and right ACA territory via ACoA and retrograde blood flow
toward right A1-ACA. Additional blood flow is from the posterior
circulation via a right hypoplastic P1-PCA into the right MCA despite
the presence of a partial fetal-type PCA.
Fig. B20.23 Extracranial duplex, longitudinal plane. Normal left CCA
flow (flow velocity: 108/32 cm/s).
Case 20 Internal Carotid Artery Dissection with Fast Recanalization
258
Degree of Neurosonologic Difficulty: Medium
Fig. B20.24 Extracranial duplex, longitudinal plane. Normalized
right CCA flow (flow velocity: 89/22 cm/s).
Fig. B20.26 Extracranial duplex, longitudinal plane. Normalizedflow
signal in right ICA (flow velocity: 58/21 cm/s).
Fig. B20.25 Extracranial duplex, longitudinal plane. Normal flow
signal in the left ICA (flow velocity: 62/24 cm/s).
Fig. B20.27 TCCS (transtemporal approach), left-sided insonation.
Normal left M1-MCA flow (flow velocity: 102/39 cm/s).
Fig. B20.28 TCCS (transtemporalapproach), right-sidedinsonation.
Normalized right M1-MCA flow (flow velocity: 72/27 cm/s).
Fig. B20.29 TCCS (transtemporal approach), left-sided insonation.
Normal left A1-ACA flow (flow velocity: 85/35 cm/s).
Discussion
259
Degree of Neurosonologic Difficulty: Medium
Fig. B20.30 TCCS (transtemporal approach), right-sided insonation.
Normalized right A1-ACA flow (flow velocity: 74/30 cm/s).
Discussion
Clinical Aspects
Here we report of a 56-year-old man who presented a
number of notable features in relation to his spontaneous
ICA dissection:
1. Dissection occurred while he was exercising in a gym.
2. Cerebral imaging revealed a right internal BZI but no
territorial infarction.
3. The first dissection-related symptoms occurred about
24 hours prior to the development of focal neurologic
deficits, which then further progressed over several
days.
4. The dissection completely recanalized within 20 days.
SimilartothepatientinCase11,thedissectioninthis
patient occurred in a gym. With careful recollection, the
majority of cases will report a suggestive “minor trauma”
which could potentially be attributed to the dissection
(Barker et al. 1976, Fisher et al. 1978, Luken et al. 1979).
Excessive physical exercise, particularly in untrained subjects can indeed considered to be a risk factor for dissection. Comparable with the patient in Case 11, this patient
had insufficient collateralization via the circle of Willis
(CW) leading to hemodynamic failure and subsequent internal BZI. In spontaneous ICA dissection, territorial infarction is a frequent finding but BZI is rare. In a large series
including 131 ICA dissections in 130 patients, BZI was
present in 5 % of cases but all of them had concurrent
embolic lesions (Benninger et al. 2004) (for further discussion on BZI, see also Chapter 4 “Arterial Ischemia,” p. 64
and Case 30, p. 338).
Our patient’s first dissection-related symptoms occurred 1 day before he developed focal neurologic signs.
Such a time delay is often observed in spontaneous ICA
dissection. A study in 42 stroke patients with ICA dissection reported prior local signs or transient ischaemic at-
Fig. B20.31 TCCS (transtemporal approach), left-sided insonation.
Unchanged normal flow in the left P1-PCA flow (flow velocity: 55/
23 cm/s).
Fig. B20.32 TCCS (transtemporalapproach), right-sided insonation.
Normal flow in the right P2-PCA (flow velocity: 62/26 cm/s). A P1PCA flow signal was no longer detectable.
tack (TIAs) in 79 % of cases. The time delay ranged from
minutes up to 31 days. However, in 82 % of patients, stroke
occurred in lessthan 1 week (Biousse et al.1995). This time
span seems to indicate the greatest embolic activity of the
dissected vessel wall.
Finally, our patient presentedrapid and complete recanalization. Vessel restitution occurs in the majority of cases,
butinmostitfinalizesafter3months.Gradualvessel
restitution can, however, start immediately, as could be
demonstrated by serial duplex ultrasound examinations
(Steinke et al. 1994) (for further discussion on spontaneous
dissection, see Case 11, p. 183).
Angiologic and Anatomic Aspects
A near occlusion of the distal ICA is a diagnostic challenge
for all imaging modalities. In contrast with proximal ICA
near occlusion which can usually be evaluated by duplex
Case 20 Internal Carotid Artery Dissection with Fast Recanalization
260
ultrasound, a confident diagnosis of a distal near occlusion
is problematic. However, a differentiation between occlusion/near occlusion and the presence of a high-grade
stenosis can be achieved by evaluating the proximal extracranial ICA flow signal. In this patient the diastolic flow
component was missing, which clearly points toward a
major distal flow obstruction (occlusion/near occlusion)
proximal to the OA origin. A residual diastolic flow would
have argued in favour of a high-grade stenosis or occlusion/near occlusion distal from the OA origin. The above
differentiations cannot be made intracranially, as a poststenotic MCA flow pattern and collateral flowvia ACoA and
PCoA may occur in ICA occlusion/near occlusion as well as
in hemodynamically relevant high-grade ICA stenosis.
Degree of Neurosonologic Difficulty: Medium
Although most ischemic events associated with cervical
artery dissection are of embolic origin, those patients with
a resulting high-grade stenosis or dissection-related ICA
occlusion might show ipsilateral hemodynamic events in
up to 16 % of cases (Steinke et al. 1996). Of particular
interest is to find out which patient with a high-grade
stenosis is at particularly high risk of developing hemodynamic ischemic stroke. The first diagnostic signs of insufficient collateralization were observed in early angiographic studies in form of a delayed ipsilateral MCA contrast filling (Boczko and Caplan 1967, Krayenbühl and
Yasargil 1982).
Standard ultrasound parameters to measure the quality
of existing collaterals in ICA occlusion are the flow velocity
and pulsatility, the systolic flow acceleration in the ipsilateral MCA as well as CVR (cerebrovascular reactivity)
(Hartmann et al. 2000, Kelley et al. 1990, Markus and
Cullinane 2001, Ringelstein et al. 1988). The latter is a
well-established and probably one of the most frequently
used functional tests to assess the risk of hemodynamic
stroke. In our case we performed the acetazolamide infusion test which revealed an ipsilateral exhausted CVR indicating insufficient intracranial collateral function.
More recently other ultrasound methods of collateral
function assessment have been described. One of these is
the ultrasound-based so-called delay test performed in
our patient (Fig. B20.15) which parallels the angiographic
delay studies described above (see also Chapter 3, “Parameters of Cerebral Hemodynamics,” p. 60). It analyzes the
hemodynamic effects of an extracranial high-grade carotid
stenosis or occlusion by simultaneous ultrasonographic
MCA echo-contrast bolus tracking (Schreiber et al. 1999).
The test directly evaluates the quality of the ACoA, PCoA, or
OAinfillingtheMCAoftheaffectedside.Itcanbeassumed
that delayed arrival of the contrast agent is directly related
to an increased flow resistance and small diameter of the
mentioned vessels. In healthy volunteers, the maximal
observed difference between the left and right sides as
assessed by this technique is 0.48 seconds. Our patient had
a delayof 1 second, which is clearlyoutside thephysiologic
range. Although prospective clinical data are not yet avail-
able, the combination of impaired CVR and a pathologic
delay test—both analyzing different parts of the cerebral
hemodynamics—probably indicate an increased risk of
hemodynamic ischemic events. Recently, the DSA delay
test was rediscovered. Yamamoto and coworkers (2004)
compared the angiographic time delay of contrast bolus
arrival between the carotid siphon and the maximal stain
of the capillary bed in 28 patients with occlusive ICA or
MCA disease. Bilateral differences (i. e., delays) were analyzed and results compared with acetazolamide single
photon emission computed tomography (SPECT). The authors found a good correlation between the techniques.
Patients with poor CVR yielded delays of up to 2 seconds
compared with 1.18 seconds in those with preserved CVR.
Other potentially useful techniques in patients with occlusive disorders of the ICA are delay analyses with contrast-enhanced MRI (Apruzzese et al. 2001, Trivedi et al.
2005) or contrast-enhanced CT (Matsumoto et al. 2007,
Waaijer et al. 2007), both using bilateral comparison of
mean transit time data. Also, noncontrast dynamic spin
labeling MRA has successfully been used (Warmuth et al.
2005). In all the above techniques a delay of 0.5–1.5 se c onds can be detected in patients with severe stenoocclusive disorders of the ICA (see also Chapter 3, “Parameters of
Cerebral Hemodynamics,” p. 60).
Patients with chronically impaired collateral function
are at particularly high risk of developing a future TIA or
stroke. Treatment strategies might therefore need to be
adapted and individualized. It may, for example, include in
ICA high-grade stenosis a carotid endarterectomy (CEA) or
stenting or the installation of an EC–IC bypass in ICA oc-
clusion (see also Case 25, p. 297).
Finally, our case demonstrated the special constellation
of a bilateral fetal-type PCA, easy to visualize on the MRA
images. However, although MRA only demonstrated a
weak connecting vessel toward the basilar artery (BA),
ultrasound revealed a turbulent flow in a small P1-PCA
segment via the distal PCA segments and via the MCA
territory, confirmed on DSA imaging. The excess flow
within this P1-PCA segment was easy to detect by transcranial color-coded sonography (TCCS) and considered as
functional stenosis. After vessel recanalization and flow
normalization no signal was detectable in the hypoplastic
P1-PCA segment. The observed cross-flow via the ACoA
was not only impaired because of a small ACoA lumen and
probably also a small lumen of the right A1-ACA segment
but also because of reduced flow from the left ICA, which
was also providing blood flow to the left ACA, MCA, and
PCA territories. This probably explains the dramatic hemodynamic impairment in this patient. It is important to
note, that a functional stenosis can not only be present in
the ACoA and PCoA but also in the P1-PCA and A1-ACA
segments in hypoplastic variants. For further discussion on
DSA, MRI techniques, and CTA in ICA dissection, see Case 11
(p.183).
Case 21
Mid-basilar Artery Occlusion
261
Clinical Presentation
A 33-year-old woman acutely developed left-sided weakness and drowsiness. In the days preceding presentation
shehadhadanoccipitalheadacheofmoderateseverity.
She had no relevant medical history and no known vascular risk factors. In particular, she had no history of migraine. Neurologic examination revealed an impaired level
of consciousness, a left-sided hemiparesis, and gaze deviation to the left (National Institute of Health Stroke Scale
[NIHSS] score 17).
Initial Neuroradiologic Findings
Initial CT 6 hours after onset of symptoms showed normal
findings, in particular no signs of subarachnoid haemorrhage (SAH). Assuming a diagnosis of basilar artery (BA)
disease, emergency digital subtraction angiography (DSA)
was performed, which revealed a severe narrowing of the
middle segment of the BA including an “intimal flap” suggestive of BA dissection. Perfusion of the posterior cerebral
artery (PCA) territory was maintained by the BA (not
shown). No interventional treatment was performed.
Suspected Diagnosis
Brainstem ischemia in the vertebrobasilar territory caused
by BA dissection.
Follow-up Neuroradiologic Findings (Day 3)
Magnetic resonance imaging (MRI) 2 days after admission
revealed multiple ischemic lesions in the vertebrobasilar
territory, particularly in the left occipital lobe, left thalamus, bilateral pontine regions, and cerebellarhemispheres
(Fig. B21.1). Three-dimensional time-of-flight (TOF) magnetic resonance angiography (MRA) demonstrated an
absentflowsignalinthemiddlesegmentoftheBA
(Fig. B21.2).
Questions to Answer by Ultrasound Techniques
• Was there occlusion or high-grade stenosis of the BA?
• Was there impaired flow in both PCAs?
Initial Neurosonologic Findings (Day 3)
Extracranial Duplex Sonography
Examination of the carotid arteries revealed normal results. The diameter of bothV2-VA segments was within the
normal range (left: 3.6mm; right: 4.4 mm). Doppler spectrum analysis showed reduced flow velocity and a mildly
increased pulsatility in both vertebral arteries (VAs)
(Figs. B21.3, B21.4).
Clinical Course (1)
Heparinization was commenced with the aim of achieving
a partial thromboplastin time (PTT) that was twofold
above normal values. Her mental status improved. Clinical
follow-up 2 days later demonstrated left hemiataxia and
mild left hemihypesthesia. In addition the patient had
right-sided hemianopia and severe dysarthria, both of
which had initially been masked by her impaired consciousness.
Transcranial Duplex Sonography
Normalflowsignalswerefoundinboththemiddle(MCA)
and the anterior (ACA) cerebral arteries.Increased velocity
and turbulent flow was detected in the right posterior
communicating artery (PCoA). The right P1-PCA segment
and the top of the BA demonstrated a reversed flow signal
while the P2-PCA segment was normal. The left P1-PCA
segment revealed a stenotic flow pattern (flow velocity:
124/83 cm/s). Slightly turbulent flow, mildly increased
flow velocities (systolic flow velocity, about 90 cm/s), and
reduced pulsatility were seen throughout the left P2- and
P3-PCA segments, suggestive of postischemic hyperemia.
Extracranial oscillation of the right internal carotid artery
(ICA) yielded positive oscillation effects in both PCAs and
in the retrograde BA, confirming collateral blood flowfrom
Case 21 Mid-basilar Artery Occlusion
262
the right ICA via the right PCoA toward the posterior
circulation (Figs. B21.5–B21.11). Transforaminal insonation revealed reduced flow velocities in both V4-VA segments, comparable with the extracranial findings. There
was a distinctly reduced flow signal in the proximalBA but
there was no signal more distally, despite the presence of
excellentinsonation conditions.Intravenous echo contrast
administration (5 mL Levovist, 300 mg/dL) confirmed the
absence of distal basilar flow. A prominent signal was seen
in the both anterior inferior cerebellar arteries (AICAs) and
in the right posterior inferior cerebellar artery (PICA)
(Figs. B21.12–B21.15).
Degree of Neurosonologic Difficulty: High
Conclusion
Mid-basilar artery occlusion distal to the AICA origin. Collateral blood flow towards both PCAs and the upper BA
segment from the right ICA via the right PCoA. In addition,
suspected left-sided P1-PCA stenosis, probablycaused by a
partially resolved embolus.
Conventional Angiography (Day 4)
One day later, DSA confirmed mid-basilar artery (BA) occlusion distal to the AICA origin, with collaterals via the
right PCoA as well as retrograde filling of the distal BA with
supply of both superior cerebellar arteries (SCAs). A left
P1-PCA stenosis was not visible (Figs B21.16–B21.19).
Figure B21.20 shows a schematic drawing of the extra- and
intracranial brain supplying arteries of the patient.
Clinical Course (2)
The etiology of the BA dissection with secondary occlusion
remained unclear. There was no history of trauma and no
findings suggestive of vasculitis or inflammatory vessel
disease. Fibromuscular dysplasia (FMD) had been excluded by DSA, and laboratory data had ruled out coagulopathy. On extensive cardiologic examination, no source of
embolism was found. Treatment was changed from heparin to aspirin. Three weeks after admission the patient
was transferred to a rehabilitation clinic, awake and with
moderate left-sided hemiataxia, right-sided hemianopia,
and cerebellar dysarthria. After 6 months the patient had
remained stable with regression of the ataxia and dysarthria. Ultrasound examination showed unchanged signs of
BA occlusion but complete regression of the left P1-PCA
stenosis (not shown).
Final Diagnosis
SpontaneousBA dissection with secondary persistentmidbasilar artery (BA) occlusion distal to the AICA origin and
consecutive multiple embolic infarcts within the vertebrobasilar artery territory.
Fig. B21.1 MR diffusion-weighted image, axial plane. Hyperintense
signals in the left occipital lobe and thalamus (A), multiple smaller
infarctions in both cerebellar hemispheres (B), and bilateralischemic
lesions in the pons (C).
Fig. B21.2 3D TOF MRA. Circle of Willis, lateral MIP. Absent flow
signal in the mid-segment of the BA (arrowhead). Note: No prominent PCoA is visible.
Final Diagnosis
263
Degree of Neurosonologic Difficulty: High
Fig. B21.3 Extracranial duplex, longitudinal plane. Reduced flow
velocity and increased pulsatility in the left V2-VA with a diameter
of 3.6 mm (flow velocity: 37/13 cm/s).
Fig. B21.5 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Circle of Willis with prominent right-sided PCoA
(arrow). Note the retrograde flow in the right blue coded P1-PCA
(arrowhead).
Fig. B21.4 Extracranial duplex, longitudinal plane. Identical flow
signal in the right V2-VA revealing a diameter of 4.4 mm (flow
velocity: 37/13 cm/s).
Fig. B21.6 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Doppler spectrum analysis in the right PCoA. Functional stenosis with increased velocity and turbulent flow (flow
velocity: 173/100 cm/s).
Fig. B21.7 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Positive oscillation effect in the right P2-PCA caused
by mild oscillation of the right extracranial ICA (flow velocity: 30/
20 cm/s).
Fig. B21.8 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Increased flow velocity in the left P1-PCA (flow
velocity: 124/83 cm/s).
Case 21 Mid-basilar Artery Occlusion
264
Degree of Neurosonologic Difficulty: High
Fig. B21.9 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Positive oscillation effect in the left P1-PCA caused
by mild oscillation of the right extracranial ICA. Note also the retrograde red-coded flow signal in the right P1-PCA (arrow).
Fig. B21.11 TCCS (transtemporalapproach), right-sidedinsonation,
upper pontine plane. Assumed distal segment of the BA demonstrating retrograde flow. Note the positive oscillation effect during
mild oscillation of the right extracranial ICA.
Fig. B21.10 TCCS (transtemporal approach), left-sided insonation,
thalamic plane. Low pulsatile turbulent flow with increased velocity
in the left distal P3-PCA (flow velocity: 87/53 cm/s).
Fig. B21.12 TCCS (transforaminal approach). Reduced flow signal in
the left V4-VA (flow velocity: 37/21 cm/s).
Fig. B21.13 TCCS (transforaminal approach). Reduced velocity in
the right V4-VA (flow velocity: 30/15).
Fig. B21.14 TCCS (transforaminal approach). Prominent flow signal
in the left AICA at a depth of 75 mm (flow velocity: 45/25 cm/s).
Final Diagnosis
265
Degree of Neurosonologic Difficulty: High
Fig. B21.15 TCCS (transforaminal approach). The color-mode im-
age reveals a prominentright-sided PICA, AICA, and proximal BA but
no distal BA signal. Note the color gap over 15 mm. The distal bluecoded signal at a depth of 95mm most likely belongs to the anterior
part of the circle of Willis and not to the distal BA. A retrograde BA
flow signal cannot be demonstrated.
Fig. B21.16 DSA,leftVAinjection,posteroanteriorview.Mid-basilar
occlusion (arrowhead). Note the prominent right PICA (arrow).
Fig. B21.17 DSA, left VA injection, lateral view. Mid-basilar occlusion. Note the cone-shaped occlusion of the BA (arrowhead), suggestive of dissection.
Fig. B21.18 DSA, right ICA injection, posteroanterior view. Filling of
both PCAs (arrowheads) from the right ICA via the PCoA.