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176
Case 10
Thrombolysis of M1 Middle Cerebral Artery Occlusion
Clinical Presentation
A 50-year-old man was admitted with a mild left-sided
weakness which had developed just 40 minutes prior to
presentation. Initial neurologic examination revealed only
a left-sided pronator drift during the arm pronation test.
No vascular risk factors were known. During emergency
computed tomography (CT) he clinically deteriorated with
progression to a high-grade hemiparesis and dysarthria
(National Institutes of Health Stroke Scale [NIHSS] score 9).
Initial Neuroradiologic Findings
Unenhancedcerebral CT showedno earlysigns of ischemia
but perfusion CT revealed severe hypoperfusion in the
right middlecerebral artery (MCA) territory with a marked
reduction in cerebral blood flow (CBF), a moderate reduction in cerebral blood volume (CBV), and a marked
delay of the mean transit time (MTT). CT angiogram
showedarightMCAocclusioninthedistalM1-MCAsegment (Figs. B10.1–B10.3).
Suspected Diagnosis
Acute MCA ischemia caused by right distal M1-MCA occlusion of unknown origin.
Initial Neurosonologic Findings
(Performed at the same time as thrombolysis was initiated.)
Extracranial Duplex Sonography
Color-coded imaging of the extracranial vessels showed no
atherosclerotic vascular changes. Doppler spectrum analysis revealed no relevant difference in bilateral flow velocities or pulsatility (not shown).
Transcranial Duplex Sonography
Color-mode insonation permitted visualization of only the
proximal part of the right M1-MCA segment while leftsided insonation was normal. Reduced flow velocity and
an increased pulsatility were seen in the right proximal
M1-MCA segment (right MCA: 20/5 cm/s, left MCA: 95/
25 cm/s) indicating distal MCA occlusion (Thrombolysis
In Brain Ischemia [TIBI] grade 2). Normal flow signals
and velocities were seen in both A1-ACA segments (flow
velocity: right: 110/45 cm/s; left: 100/40 cm/s) and the PCA
on both sides (Figs B10.4–B10.7).
Conclusion
Right distal M1-MCA occlusion of unknown etiology.
Clinical Course (1)
After exclusion of contraindications, intravenous thrombolysis with 75 mg recombinant tissue plasminogen activator (rt-PA) was commenced 1.5 hours after the onset of
symptoms.
Questions to Answer by Ultrasound Techniques
• Was there evidence of atherosclerosis in the extracranial
brain-supplying arteries?
• Could there be a sustained occlusion of the right MCA?
• Ifso,wasthereevidenceofcollateralbloodflowviathe
anterior cerebral artery (ACA) and posterior cerebral
artery (PCA)?
Figure B10.8 shows a schematic drawing of the extra- and
intracranial brain-supplying arteries.
Clinical Course (2)
During thrombolysis the neurologic status of the patient
improved steadily.
Follow-up Neurosonologic Findings (1 Hour)
Transcranial Duplex Sonography
At 70 minutes after initiation of rt-PA infusion, color-mode
insonation showed a normalized M1-MCA segment, now
visible over its total length. Doppler spectrum analysis
revealed an improved flow (flow velocity: 55/20 cm/s). In
comparison to the initial TCCS, flow velocity in the right
A1-ACA segment had decreased (flow velocity: 75/35 cm/
s) indicating an initial leptomeningeal collateralization
(Figs. B10.9, B10.10).
Conclusion
Partial M1-MCA recanalization after intravenous rt-PA infusion with signs of residual peripheral flow obstruction.
Final Diagnosis
Final Diagnosis
Cardioembolic occlusion of the right distal M1-MCA segment with recanalization after intravenous thrombolysis
with rt-PA.
177
Clinical Course (3)
Clinical improvement continued further until there was a
mild residual left-sided hemiparesis (NIHSS score 3).
Transesophageal echocardiography (TEE) shortly after intravenousthrombolysisshowedtwosmallfloatingstructures adjacent to the aortic valve. Heparinization, aiming
for a twofold rise in partial thromboplastin time (PTT), was
initiated after 24 hours. Follow-up CT 1 day later showed a
small cortical/subcortical infarction mainly in the right
posterior insular region. No hemorrhagic transformation
was seen (Fig. B10.11). Follow-up TEE after 4 days demonstrated complete normalization. Negative blood cultures and absence of systemic infection signs made endocarditis unlikely. A transient cardiac thrombus was suspected, and continuous oral anticoagulation with phenprocoumon was initiated.
Degree of Neurosonologic Difficulty: Low
Fig. B10.1 Unenhanced cranial CT, axial plane. No early signs of
ischemic brain damage.
Fig. B10.2 Perfusion CT, rCBF, rCBV and MTT
maps axial planes. Severe hypoperfusion in the
right MCA territory. CBF/CBV mismatch indicating tissue at risk within the right MCA-territory. A Decreased cerebral blood flow (CBF)
(arrows). B Mildly reduced cerebral blood volume (CBV). C Delayed mean transit time
(MTT).
Case 10 Thrombolysis of M1 Middle Cerebral Artery Occlusion
178
Degree of Neurosonologic Difficulty: Low
Fig. B10.3 Intracranial 3D CTA, axial MIP. Occlusion of the distal
right M1-MCA segment (arrowhead).
Fig. B10.5 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Reduced flow velocities (20/5 cm/s) and increased
pulsatility in the proximal right M1-MCA indicating distal MCA occlusion (TIBI grade 2).
Fig. B10.4 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow signal in the left M1-MCA (flow velocity:
95/25 cm/s).
Fig. B10.6 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal flow signal in the left A1-ACA (flow velocity:
100/40 cm/s).
Discussion
Fig. B10.7 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Normal flow signal in the right A1-ACA (flow velocity: 110/45 cm/s).
Clinical Aspects
Here, we report on a 50-year-old stroke patient who initially presented with a mild left-sided hemisyndrome
which progressed after 70 minutes to high-grade hemiparesis. He received intravenous rt-PA thrombolysis 90
minutes after the onset of symptoms. The underlying
cause was a cardiac embolism.
Intravenous rt-PA thrombolysis is currently the only
approved causal therapy of acute stroke. The recommendations of the various neurologic societies are based on the
results of the American National Institute of Neurological
Disorders and Stroke (NINDS) study, published in 1995
(The NINDS rt-PA Stroke Study Group 1995). This was a
randomized placebo-controlled trial in 624 patients, and
demonstrated that patients treated with rt-PA had a better
Fig. B10.8 Schematic drawing of the extra- and intracranial brainsupplying arteries of the patient in Case 10. Note the right distal M1MCA occlusion (circle). Leptomeningeal collateralization of the right
MCA territory via the right ACA (red arrow).
Discussion
Fig. B10.9 TCCS (transtemporal approach), right-sided insonation,
midbrain plane. Color-mode delineation of the complete M1-MCA
without discontinuation. Ameliorated flow signal with a flow velocity
of 55/20 cm/s.
179
Degree of Neurosonologic Difficulty: Low
Fig. B10.10 TCCS (transtemporalapproach), right-sided insonation,
midbrain plane. Normalization of right A1-ACA flow indicating regression of initial flow increase via leptomeningeal collaterals (flow
velocity: 75/35 cm/s).
clinicaloutcome at3 months compared with controls. This
was true, despite a higher frequency of symptomatic intracranial bleedings under rt-PA treatment (rt-PA: 6.4 % vs.
placebo: 0.6 %). Treatment was commenced within a time
window of 0–3 hours after the onset of symptoms. After
publication of this study, the US Food and Drug Administration (FDA) approved rt-PA treatment within the above
time window for patients with acute stroke. The European
Cooperative Acute Stroke Study ECASS-I, also published in
1995, could not confirm the positive results of the NINDS
study. In this trial, the time window had been extended to
Fig. B10.11 Unenhanced cranial CT,axial plane. Follow-up CTafter 1
day: Small cortical/subcortical infarction mainly in the right posterior
insular region (arrows).
6 hours (Hacke et al. 1995). Since then two other rt-PA
trials have been published which analyzed different time
windows (ECASS-II: 0–6 hours; Alteplase Thrombolysis for
Acute Stroke Noninterventional Therapy in Ischemic
Stroke [ATLANTIS] 3–5hours)andwhichfailedtoshowa
significant improvement in generalclinical outcome(Clark
et al. 1999, Hacke et al. 1998).
In recent years, the results of the published trials have
been studied in a number of metaanalyses. Hacke and
coworkers (1999) reported a combined analysis of NINDS
and the ECASS trials that revealed the occurrence of a bad
Case 10 Thrombolysis of M1 Middle Cerebral Artery Occlusion
180
clinical outcome was reduced despite the increased rate of
symptomatic bleedings. Mortality, however, remained unchanged. Thenumber needed totreat to prevent 1 deathor
disability for the 3-hour inclusion window was 7 and for
the 6-hour inclusion window it was 11. A further study
confirmed the increased risk of bleeding, but the risk was
clearly outweighed by the benefits of treatment. Again,
most benefits were seen within the 3-hour time window.
In addition, rt-PA demonstrated the best risk–benefit ratio
when different thrombolytic agents were compared
(Wardlaw et al. 2002).
In 2004 another metaanalysis was published that also
Degree of Neurosonologic Difficulty: Low
included the results of the ATLANTIS trial. Here, the influence of treatment delay was analyzed, specifically looking
at the bleeding complications and the clinical outcome at
90 days. It revealed a decreasing chance of a good outcome
with increasing time to the onset of treatment. Best results
were achieved if treatment was commenced within 90
minutes. Within the time window of 271–360 minutes,
no significant benefit in clinical outcome could be observed (Hacke et al. 2004). The pooled data revealed additional information: Patients with a severe neurological
deficit also seemed to benefit from a later onset of treatment, while patients with a small deficit had a significantly
higher chance of achieving an excellent clinical outcome
(Gonzales et al. 2006). On the basis of the currently available data, systemic thrombolysis can clearly be recommended. The achievable benefit is largest within 90 minutes and decreases with increasing time delay between
onset and the beginning of treatment. Regarding the selection criteria for thrombolysis, we recommend the
methods suggested by the neurologic societies, such as
the “Guidelines for the Early Management of Patients
with Ischemic Stroke” of the American Heart Association/
American Stroke Association (Adams et al. 2007).
Unfortunately, the use of the above therapeutic approach is still limited. A number of surveys have demonstratedthat only2 % of patientsin generalhospitals and 5 %
in locations with an available stroke unit are treated with
thrombolysis (Heuschmann et al. 2004). One of the reasons for this is the fear of bleeding complications. Another
major problem is the delayed presentation of patients to
hospital or unknown time of symptom onset. Finally, some
clinicians have raised doubts as to whether the positive
results achieved under study conditions in specialized
centers can be transferred into everyday practice.
Although data are contradictory, the recently published
Safe Implementation of Thrombolysis in Stroke Monitoring Study (SITS-MOST)—a European observational study in
6483patientsfrom14countries—demonstrates that re-
sults comparable with the NINDS trial can be achieved
even if centers with little experience in thrombolysis are
included (Wahlgren 2007). Results of the ongoing studies
(ECASS-III, International Stroke Trial-3 [IST-3]) will further
help to clarify this issue.
Intraarterial thrombolysis is even less frequentlyused in
clinical practice. Its advantage is the higher local concen-
tration of the thrombolytic agent and less systemic action,
which is why it is more effective and safe. Disadvantages
are the high technical requirements that restrictits use to a
few specialized centers. In the PROACT II study (Prolyse in
Acute Cerebral Thrombombolism) intraarterial urokinase
was given within 6 hours of stroke onset. In comparison
with heparin alone, substantially better recanalization of
occlusions (66 % vs. 18 %, respectively) as well as a better
clinical outcome, assessed after 90 days, were observed
(Furlan et al. 1999). A combination of intravenous and
intraarterial thrombolysis, the so-called “bridging technique,” is currently the subject of intensive research.
Apart from its use for diagnostic purposes, ultrasound
has recently been shown to have a therapeutic potential.
Ultrasound is able to cause changes within the fibrin structure of a thrombus by inducing plasma “microstreams.”
This subsequently leads to better penetration and action of
rt-PA. Both mechanisms accelerate thrombolysis. In 2004
the results of the Combined Lysis of Thrombus in Brain
Ischemia with Transcranial Ultrasound and Systemic TPA
(CLOTBUST) study were published, which included 126
patients with acute proximal or distal MCA occlusion.
Thepatientswererandomizedtoeitherrt-PAtreatment
alone or a combination of rt-PA and continuous transcranial Doppler (TCD) with a diagnostic 2 MHz transducer
over 2 hours. Patients treated with the combined approach
demonstrated a much higher rate of early recanalization
within2hours(46%vs.18%)andatrendtowardadistinct
clinical improvement (29 % vs. 21%). The trend persisted
after 3 months. The study was underpowered, however, to
demonstrate a statistically significant difference (Alexandrov et al. 2004). A single-center transcranial color-coded
sonography (TCCS) study in 37 patients with MCA main
stem occlusion also demonstrated a higher recanalization
rate if continuous ultrasound was applied over 1 hour
(46 % vs. 21 %, respectively). However, the number of patients was again too small for a sensible statistical analysis
(Eggers et al. 2003).
To improve ultrasound penetration and therefore the
thrombolytic effect of ultrasound, the effects of low-frequency ultrasound (300 KHz) were analyzed in acute
stroke patients undergoing intravenous thrombolysis. Unfortunately, this approach resulted in substantially higher
numbers of intracranial hemorrhage and the study had to
be terminated early (Daffertshofer et al. 2005).
Another potential approach that could enhance ultrasound-induced thrombolysis is the use of air or gas-filled
“microbubbles,” i.e., ultrasound contrast agents. A recent
pilot study has already shown the positive effect of combining TCD ultrasound, microbubble, and rt-PA treatment,
compared with combined TCD and rt-PA or rt-PA alone
(Molina et al. 2006).
Finally, sonothrombolysis alone, i. e., the use of diagnostic transcranial ultrasound for therapeutic purposes, has
been proposed. This is of particular interest in light of the
many patients who cannot have rt-PA thrombolysis due to
thepresenceofcontraindications.Apilotstudyinpatients
Discussion
181
with MCA main stem occlusion with a 6-hour inclusion
time window demonstrated recanalization in 62.5 % of
patients with 1 hour of continuous TCCS compared with
no recanalization in the noninterventional group (Eggers
etal.2005).Amulticenterstudy,TRUSCA(Thrombolysis
with Ultrasound in Contradiction for Alteplase), addressing this issue is currently planned (Eggers and Valdueza
2007b).
Further study results in the field of sonothrombolysis
with TCCS and intravenous rt-PA thrombolysis TRUST
(Transcranial Ultrasound Enhanced Thrombolysis) and
with TCD and intravenous rt-PA with a new echo contrast
agent (TUCSON Transcranial Ultrasound in Clinical SONlysis) are awaited.
Angiologic and Anatomic Aspects
Currently, the selection of patients for thrombolysis is
solelybasedontheexclusionofanintracerebralhemorrhage using cranial CT. Knowledge of the vascular status or
the tissue at risk is not required to make a therapeutic
decision. But not all patients with clinical symptoms of
stroke actually have an occlusion of a major brain-supplyingarteryorevenanocclusionthatcouldpotentiallybe
reopened by thrombolysis. This patient group, however, is
exposed to the 5–10 % risk of an intracranial bleed. A major
argument against an extended vascular diagnosis has been
the time factor. But with the increasing availability of
multimodal CT and magnetic resonance imaging (MRI) as
well as ultrasound techniques, which permit a fast and
reliable diagnosis of vessel occlusions, the vascular status
can now be obtained without relative delay. This in turn
will help to stratify patients early and subsequently allow
the administration of individualized treatment strategies,
probably leading to better clinical outcomes.
The most advanced technique to date is modern MRI. If
perfusion and diffusion weighted images are used, brain
tissue that is functionally but not yet structurally impaired—called the penumbra—can be visualized. From this
technique the so-called “mismatch concept” has been developed and successfully applied to select patients for
thrombolysis. The DIAS (Desmoteplase In Acute Stroke)
and DEDAS (Dose Escalation Study of Desmoteplase in
Acute Ischemic Stroke) studies showed considerable improvement of early reperfusion as well as of the clinical
outcome (Hacke et al. 2005, Furlan et al. 2006). The results
oftheDIASIIstudyhavenotbeenpublishedsofar.A
similar approach is followed in current CT perfusion studies. The CT technique is of particular logistical advantage as
CT access for emergency patients is usually easy to obtain.
Using CT, the ischemic penumbra or “tissue at risk” can be
defined as the difference between the CBF (in analogy to
perfusionMRI)andtheCBV(inanalogytodiffusionMRI).
An initial comparative study in 42 stroke patients was
recently published and showed that tissue at risk determined by perfusion CT and CTA was equivalent to the MRI
resultsinallbutonecases(Wintermarketal.2007).Fi-
nally, ultrasound perfusion tests have also been performed
in acute stroke patients. Ultrasound follows the same basic
approach of MRI and CT,analyzing the perfusion kinetics of
a contrast bolus within the microcirculation. However, for
several reasons, this technique is currently still experimental and rather limited (Meyer-Wiethe et al. 2007).
Digital subtraction angiography (DSA) is so far the reference method for the evaluation of intracranial occlusions.
In clinical practice, multislice CTA, yielding similar results,
is increasingly being used. In basilar artery (BA) pathology,
CTA sensitivity is even higher as it has been shown to
detect distal BA near occlusions that were considered to
be complete occlusion by DSA. After correction of the
false-positive BA occlusions the sensitivity, specificity,
and positive and negative predictive values for the detection of intracranial occlusions of the major arteries by CTA
were 100 %, 10 0 %, 100 %, and 10 0 % , res pec tively. Respective values for time-of-flight (TOF) MRA in the same patient group were 87 %, 98 %, 59 %, and 99.5 %, respectively
(Bash et al. 2005). The latter findings contradict earlier TOF
MRA sensitivity and specificity results of 100 % and 95 %
(Stock et al. 1995). When analyzing more distal artery
occlusions the limitation of TOF MRA becomes even
more evident. Using contrast-enhanced MRA 20 % of
main stem arteries or their branches were patent, which
had been interpreted as occluded by TOF MRA (Yang et al.
2002). The spatial resolution of TOF MRA can be improved
if 3 T and sensitivity-encoding techniques are combined.
This has been shown to improve the diagnostic results.
Compared with DSA, sensitivity, specificity, and positive
and negative predictive values of 100 %, 99 %, 87 %, and
100 %, respectively, were reported but the authors included MCA and internal carotid artery (ICA) occlusions
only (Choi et al. 2007).
CT and MRI can mainly be used as “single shot” methods.
For continuous monitoring they are either too laborious,
too expensive, or place too much strain on the patient. In
comparison, ultrasound has the advantage of permitting
serial as well as continuous measurements without the
above restrictions. TCD in the hands of an experienced
sonographer may allow diagnosis of main stem occlusion,
for example of the MCA. If applied in acute stroke patients,
however, TCCS is the superior method, especially if ultrasound contrast agents are used. In 20 of the 23 patients
contrast-enhanced TCCS was able to correctly diagnose
intracranial vascular pathology while TCD and unenhanced TCCS were only successful in 14 and 7 patients,
respectively (Görtleretal.1998).InTCDthisiscausedby
the lack of spatial information.
Using TCCS, provided that the transcranial bone window
is sufficient or signals are enhanced by contrast agents, the
diagnosis of a proximal MCA occlusion is simple if color
signal and Doppler spectrum in projection of the artery in
question are absent. In a small study of 10 stroke patients
withamainstemocclusionoftheMCAdiagnosedbyTOF
MRA, TCCS confirmed the diagnosis in all (Kenton et al.
1997). TCCS detection of single MCA branch occlusion is
Degree of Neurosonologic Difficulty: Low
Case 10 Thrombolysis of M1 Middle Cerebral Artery Occlusion
182
usually impossible because of the unknown number of
branches in the individual patient. Occlusion of more
than one branch, however, can be considered if a relevant
difference in blood flow velocity is present between the
right and left sides (for further discussion on bilateral
differences in branch occlusion and asymmetry index of
Zanette,seeCase13,p.204).Proximalocclusionsmayalso
result in detectable indirect hemodynamic signs, for example, an M1-MCA occlusion may cause raised flow velocities in the ipsilateral ACA and PCA, indicating their function as feeders of leptomeningeal collateral vessels (see
also chapter 5, Fig. A5.48). It can be difficult however to
Degree of Neurosonologic Difficulty: Low
differentiate collateral flow from additional stenosis, or to
confirm the presence of both.
The diagnostic accuracy of TCCS in hyperacute stroke in
comparison to CTAand MRA was recently analyzed. A total
of 58 stroke patients were examined within the first 6
hours of stroke onset by unenhanced and if necessary by
subsequent contrast-enhanced extra- and intracranial duplex ultrasound. Examination was performed before initiation of other diagnostics while the patient was still in
the emergency room. Echo-contrast use was considered
necessary in 51 patients. Mean duration of complete examination was 21.3 minutes in combined native and contrast-enhanced examination and 13.6 minutes if native
examination was performed alone. Ultrasound findings
couldbeconfirmedbyDSAin31of32patients(Gerriets
et al. 2002). Shorter examination times could probably be
achieved if contrast agents were administered rather at
thebeginningoftheultrasoundexamination.TCCSalso
allows assessment of vessel recanalization. In patients
receiving intravenous rt-PA, recanalization of MCA main
stem occlusion was seen in 50 % after 2 hours and in 75 %
after 24 hours. In conservatively treated patients the same
study found no recanalization within 2 hours and in only
8 % after 24 hours (Gerriets et al. 2000).
Acute MCA occlusions differ from chronic occlusions as
in the former rapid changes of findings may frequently be
observed over a short period. Occlusions might be incomplete, and subsequent flow normalization and re-occlusion might be seen within a few minutes of continuous
observation. To evaluate the different types of observable
flow profiles, a grading system between 0 and 5 (TIBI
criteria) characterizing flow in MCA and BA in stroke has
been introduced (Demchuk et al. 2001). A TIBI grade 0–1
(absent—minimal) corresponds to a complete MCA main
stem occlusion and TIBI 2–3(blunted—dampened) is
found in distal M1-MCA occlusion. TIBI 4 indicates a stenosis during advanced recanalization and TIBI 5 equals normal flow, for example, after complete recanalization (for
further reading see also chapter 5, “ Intracranial Pathology,” p. 94). This grading system, although controversial,
is a first step to describing the dynamic processes that
occur during recanalization. Further improvement is to
be expected if this systemis transferred toand reevaluated
by TCCS. Flow velocity differences between the right and
left sides can furthermore be analyzed and described by a
number of asymmetry indices (see also Case 13, p. 204).
Initial application of the above criteria in acute stroke
patients has revealed valuable information. It was demonstrated that recanalization of embolic occlusions follows
different temporal patterns. According to Alexandrov and
coworkers (2001), embolic occlusions can be divided into
three main recanalization types: those that recanalize
within 1 minute of rt-PA treatment initiation, those that
need 1–29 minutes, demonstrating stepwise recanalization, and those that need more than 30 minutes. Correlation with stroke etiology demonstrated that quick recanalization occurs in 59 % of cardioembolic MCA occlusions
but in only 8% of atherothrombotic artery-to-artery occlusions. Fast recanalization in patients with stroke of undetermined origin occurred in 50 % of cases, suggesting that
most of these might actually be of cardioembolic origin
(Molina et al. 2004).
Furthermore, the TIBI grades can be used for early assessment of stroke prognosis. A low initial TIBI grade significantly correlates with bad clinical outcome and a
higher mortality (Demchuk et al. 2001). Sudden recanalization has better clinical prognosis (Alexandrov et al.
2001). TCCS assessment of recanalization in the multicenter Neurosonolgy in Acute Ischemic Stroke (NAIS) study
(361 patients) confirmed that a persisting MCA main stem
occlusion 6 hours after onset of symptoms was an independent predictor for poor clinical outcome. After 3
months, 88 % of these patients had died or were dependent, while patients with a distal branch occlusion or normal ultrasound findings demonstrated a good clinical outcome in 50 % and 63 %, respectively (Allendoerfer et al.
2006). The assessment of collateral flow, i. e., the ACA
and PCA flow in MCA occlusion may further help to evaluate prognosis. As expected, patients with good collateral
flow in persisting MCA occlusion have a better clinical
outcome (Kim et al. 2005).
Finally, continuous monitoring helps in the understanding of the secondary clinical worsening of acute stroke
patients. This is frequently seen and is often caused by
an early reocclusion. A systematic analysis in 374 patients
undergoing systemic thrombolysis demonstrated early reocclusion in 14% of cases, which was mostly associated
with a clinical worsening (Saqqur et al. 2007).
Case 11
Secondary Occlusion in Internal Carotid Artery Dissection
183
Clinical Presentation
A 43-year-old man complained of transient right-sided
weakness, amnesic aphasia, and decreased visual acuity
in his left eye that started whilst he was undertaking mild
exercise in a gym. The symptoms gradually faded over 15
minutes. The patient had no vascular risk factors except for
a known migraine with aura. On admission to our hospital
he was free of symptoms. Headaches were not reported.
The neurologic examination revealed a mild left-sided
Horner syndrome. There were no other focal neurologic
deficits.
Initial Neuroradiologic Findings
Cerebral magnetic resonance imaging (MRI) on the day of
admission showed no ischemic parenchymal lesion but
perfusion imaging revealed a pronounced hypoperfusion
within the left middle cerebral artery (MCA) territory and
both anterior cerebral artery (ACA) territories. Time-offlight (TOF) magnetic resonance angiography (MRA)
showed reduced signal intensity in the left distal internal
carotid artery (ICA), left MCA, and both ACAs, as well as an
aplasia of the right A1-ACA segment and both posterior
communicating arteries (PCoAs) (Figs.B11.1–B11.3). The
cervical vessels were not examined.
Suspected Diagnosis
Dissection of the left ICA.
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode ultrasound did not show atherosclerosis or other
structural vessel abnormalities. Color-mode imaging of the
left ICA demonstrated a tapering lumen and reduced color
signal intensity. Doppler spectrum analysis revealed a
pronounced reduction of flow velocity and mild increased
pulsatility in contrast with the contralateral side
(Figs. B11.4, B11.5). The external carotid artery (ECA) had
an increased diastolic, i. e., an “internalized,” blood flow.
Assessment of the vertebral arteries (VAs) was normal.
Transcranial Duplex Sonography
A poststenotic flow pattern was observed in the left carotid
siphon,theleftM1-MCAsegmentaswellasintheleft
A1-ACA segment. No right A1-ACA segment and no flow
signal in the presumed area of both PCoAs were detected.
The flow direction in the left OA was reversed and showed
a high diastolic flow component similar to that of a brainsupplying artery. The right OA was normal. Assessment of
the posterior circulation was unremarkable and without
evidence of collateral leptomeningeal flow (Figs. B11.6–
B11.11).
Conclusion
Suspected dissection of the left ICA with high-grade stenosis of hemodynamic relevance below the OA origin. Insufficient intracranial collateral blood flow towards the left
MCA and both ACA territories solely via the left OA.
Questions to Answer by Ultrasound Techniques
• Was there evidence of dissection, high-grade stenosis,
or occlusion of the ICA?
• Ifso,wasthereevidenceofcollateralbloodflowviathe
ACA, PCoA, ophthalmic artery (OA), or leptomeningeal
vessels via the posterior cerebral artery (PCA)?
Clinical Course (1)
On the basis of the above findings, intravenous heparin
was started, aiming for a twofold rise of partial thromboplastin time (PTT). During the patient’sfirstnightinhospital, he developed a severe right-sided brachiofacial paresis and a global aphasia. Laboratory monitoring revealed
a fourfold increase in PTT. Intracranial bleeding was ruled
out by a computed tomography (CT) scan.
Case 11 Secondary Occlusion in Internal Carotid Artery Dissection
184
Questions to Answer by Ultrasound Techniques
• Was the clinical worsening caused by a thromboembolic
event with secondary occlusion of distal MCA branches
or by hemodynamic impairment due to stenosis progression or occlusion of the ICA?
• If an occlusion of the ICA was present, which collateral
pathways were activated in comparison with the initial
investigation?
Degree of Neurosonologic Difficulty: Medium
Follow-up Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
B-mode image of the left ICA remained unchanged. However, Doppler spectrum analysis now demonstrated a high
resistance flow signal with a low and short systolic flow
and completely absent diastolic flow component
(Fig. B11.12).
Transcranial Duplex Sonography
A worsened poststenotic flow pattern was observed in the
left M1-MCA and A1-ACA segments. Furthermore, there
was an increase of retrograde flow in the left OA. Raised
flow velocity in the left P2/3-PCA segments, previously not
observed, indicated leptomeningeal collateral flow from
the PCA to the left anterior territory (Figs. B11.13–B11.16).
Conclusion
Secondary distal occlusion of the left ICA. Further worsening of the preexisting insufficient blood flow in the left
MCA and both ACA territories. Collateralization via the left
OA and in addition via leptomeningeal collaterals from the
left PCA.
border zone infarction between the left ACA and MCA
territories (Fig. B11.19).
Follow-up Neurosonologic Findings (Day 7)
Extracranial Duplex Sonography
Partial reopening of the left ICA was seen, now demonstrating a flow signal similar to that on day 1 (Fig. B11.20).
Transcranial Duplex Sonography
A continuing poststenotic flow pattern was seen within
the left M1-MCA and A1-ACA segments. However, flow
velocities had slightly increased. The OA flow was still
reversed indicating a persisting hemodynamically relevant ICA obstruction below the origin of the OA
(Fig. B11.21).
Conclusion
Partial reopening of the distal ICA with a remaining hemodynamically relevant high-grade stenosis. The result is
equivalent to the neurosonologic findings on admission.
Clinical Course (3)
Treatment was changed from heparin to continuous oral
anticoagulation with Phenprocoumon. Three weeks following admission the patient was clinically stable and
was discharged with a moderate right-sided paresis and
motor aphasia.
Follow-up Neurosonologic Findings (6 Months)
Figure B11.17 shows a schematicdrawing of the extra- and
intracranial brain-supplying arteries.
Clinical Course (2)
Computed tomographic angiography (CTA) was performed, which demonstrated a left intracranial ICA occlusion in its petrosal part. The beginning of the dissection
was assumed to be located in the midcervical extracranial
ICA (Fig. B11.18). None of the studied intra- and extracranial arteries showed evidence of fibromuscular dysplasia.
Under hypervolemic treatment the aphasia and the hemiparesis improved slowly over subsequent days. Six days
following admission, cerebral MRIrevealed a large internal
Extracranial Duplex Sonography
The left ICA had normalized (Fig. B11.22).
Transcranial Duplex Sonography
The left MCA and ACA as well as the PCAs demonstrated
normalized flow velocities and pulsatility. The flow direction of the left OA was now orthograde (Figs. B11.23–
B11.26).
Conclusion
Flow normalization in the left ICA without signs of intracranial collateral blood flow, indicating hemodynamic normalization.
Final Diagnosis
Final Diagnosis
185
Spontaneous dissection of the left ICA in a patient with
unfavorablecircleofWillis(CW)collateralizationduetoa
nonfunctional right A1-ACA and nonfunctional bilateral
Fig. B11.1 MRI, apparent diffusion coefficient (ADC) map, axial
plane. No signs of cytotoxic edema.
PCoAs. Secondary transient occlusion, presumably triggered by anticoagulation with intravenous heparin, leading to internal border zone infarction.
Degree of Neurosonologic Difficulty: Medium
Fig. B11.2 MR T2* perfusion image, (time-to-peak map) axial
plane. Pronounced hypoperfusion within the left MCA and both
ACA territories.
Fig. B11.3 3D TOF MRA, axial MIP. Reduced signal intensity in the
left intracranial ICA (arrows), left MCA, and both ACAs. Note the
missing signals in the right A1-ACA (arrow) and the PCoAs, suggesting aplasia.
Fig. B11.4 Extracranial duplex, longitudinal plane. Tapering vessel
size and pronounced reduction of blood flow in the left ICA distal of
the bifurcation (flow velocity: 28/8 cm/s).