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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5773_Библиотеки_им_академика_М_И_Перельмана.pdf
Case 19 Vertebral Artery Dissection with Distal Occlusion
246
Clinical Course
The clinical development of the right-sided cerebellar
syndrome changed the differential diagnosis from a vestibular neuropathy to a cerebellar ischemia. On the basis of
our subsequent findings a spontaneous VA dissection was
assumed. Initially intravenous partial thromboplastin time
(PTT)-guided heparinization was commenced, which was
later changed to oral anticoagulation with phenprocoumon. The patient was discharged with mild right hemiataxia. A follow-up MRI 6 months later showed no new
ischemic events, and cervical MRA revealed a persisting VA
Degree of Neurosonologic Difficulty: Medium
occlusion. Clinically the patient had further improved.
Treatment was changed to long-term antiplatelet therapy
with aspirin. Ehlers–Danlos syndrome was excluded by a
skin biopsy.
Final Diagnosis
Right PICA infarction caused by spontaneous dissection
and occlusion of the right VA proximal to the PICA origin.
Fig. B19.1 Cerebral MR FLAIR image, axial plane. Subacute large
cerebellar ischemic lesion in the right PICA territory.
Fig. B19.3 Extracranial duplex, longitudinalplane. Left V2-VA diameter: 3.9 mm.
Fig. B19.2 3D TOF MRA, coronal MIP. Absent signal in the distal right
VA. Note the missing P1-PCA (arrow) on the left side indicating fetaltype variant of PCA.
Fig. B19.4 Extracranial duplex, longitudinal plane. Normal left V2VA flow signal (flow velocity: 54/27 cm/s).
Final Diagnosis
247
Degree of Neurosonologic Difficulty: Medium
Fig. B19.5 Extracranial duplex, longitudinal plane. Large anecho-
genic zone in the right V2-VA probably reflecting mural hematoma
(arrowheads). Residual vessel lumen: 2.6 mm. Note the regular
proximal V2-VA diameter of about 3 mm.
Fig. B19.7 Extracranial duplex, longitudinal plane. High-resistance
flow signal with low and short systolic flow and completely absent
diastolic flow component in the right V2-VA suggestive of VA occlusionbelowthePICAorigin(flowvelocity15/0cm/s).
Fig. B19.6 Extracranial duplex, longitudinal plane. Residual perfused lumen of the right V2-VA further distal: 1.7 mm.
Fig. B19.8 TCCS (transforaminal approach). Normal flow signal in
the left V4-VA (flow velocity: 55/38 cm/s).
Fig. B19.9 TCCS (transforaminal approach). Reduced retrograde
flow signal in projection of the right V4-VA (flow velocity: 25/
11 cm/s).
Fig. B19.10 TCCS (transforaminal approach). Normal flow signal in
the BA at a depth of 81 mm (flow velocity: 60/32 cm/s).
Case 19 Vertebral Artery Dissection with Distal Occlusion
248
Degree of Neurosonologic Difficulty: Medium
Fig. B19.11 DSA, right VA injection, posteroanterior view. Varia-
tions in caliber in the V2-VA and long-segmented filiform stenosis
in its distal V2-VA part and proximal V3-VA segment suggestive of
dissection (arrowheads). Note several small vessels, originatingfrom
the right V2-VA (arrows).
Fig. B19.13 DSA, left VA injection, posteroanterior view. Intimal flap
mild dilatation in the left mid V2-VA segment (arrowhead).
Discussion
Clinical Aspects
Here we discuss a 29-year-old woman who had acute
vertigo in combination with nausea and vomiting, leading
to the initial diagnosis of a left-sided vestibular neuro-
Fig. B19.12 Follow up, late-phase DSA image of the area shown in
Figure B19.11. Complete interruption of flow within the distal V3-VA
segment (arrowhead).
pathy. However, detailed neurologic examination on the
following day revealed additional mild cerebellar signs
consisting of spontaneous and gaze-evoked nystagmus
to the right, a right-sided drift, and an impaired suppression of vestibular nystagmus; the head thrust test was
normal on both sides. MRI subsequently confirmed subacute cerebellar ischemia within the PICA territory.
Dizziness and vertigo are common but unspecific symptoms which might be caused by several diseases seen in
the fields of general internal medicine, ENT or neurology. It
is not uncommon that a neurological patient is treated
with a presumed gastroenteritis and myocardial infarction
before being attended by a neurologists. Even in neurological wards in cases of acute vertigo, differentiation between peripheral and central vestibular causes may be
difficult. Cerebellar and, in particular, PICA infarctions
might clinically present with the symptoms of a peripheral
vestibular syndrome. The PICA supplies the key regions of
the vestibulocerebellar system with its connections to the
ipsilateral vestibular core regions, which may result in a
predominantly vestibular pattern of PICA failure. Signs of
ataxia may be faint or even absent. Up to 17 % of patients
with PICA infarction present with the clinical symptoms of
a pure vestibular neuropathy. The most helpful criterion
for differentiation was the head thrust maneuver and the
caloric test result as all patients with PICA infarction demonstrated normal findings (Lee Lee et al. 2006). In most
cases, however, acute vertigo, nausea, vomiting, and an
unsteady gait are the main symptoms of PICA infarction,
and then only a detailed neurologic examination might
reveal additional signs indicative of a central vestibular
Discussion
249
syndrome. In the event of doubt, cerebral MRI should be
performed, so that cerebral ischemia is not missed.
In our presented case, PICA infarction was the result of a
distal VA occlusion caused by spontaneous extracranial VA
dissection. An arterial dissection is an important differential diagnosis that needs to be considered as it is a cause
of stroke inyoung patients in up to 25 % of cases (Schievink
2001). A dissection usually occurs as a result of an intimal
lesion with subsequent bleeding and development of an
intramural hematoma within the layers of the arterial
vessel wall. A more subintimal location will result in a
narrowing of the vessel lumen or occlusion while a more
subadventitial location results in the development of
aneurysms. Further potential risk factors in our patient
were the history of migraine and a recent upper respiratory tract infection (for further discussion on pathogenesis
and the role of migraine, see Case 11, p.183). Recent infection, predominantly of the upper respiratory tract, has
been associated with cervical artery dissection. In a study
of young stroke patients (below 50 years of age), recent
infection was significantly more common in patients with
vessel dissection (58.1 % vs. 32.8 % with no dissection)
(Grau et al. 1999). Similar results were found in a study
that compared 47 dissection patients (31.9 %) and 52 patients with stroke of other etiology (13.5 %) (Guillon et al.
2003). Another potential risk factor for VA dissection is
chiropractic manipulation. In a large clinical series, 30 % of
patients with VA dissection reported prior cervical spine
manipulation compared with 6 % with ICA dissection. The
time delay between manipulation and clinical symptoms
variedfromsecondsupto10days(Dziewasetal.2003).
However, prior chiropractic treatment was denied by our
patient. Furthermore, we found no evidence of systemic
vascular disease and DSA could not confirm signs of FMD.
Ehlers–Danlos syndrome was considered but excluded by
askinbiopsy.
Spontaneous VA dissection without clinical symptoms is
rare. In a recent study of 195 VAdissections in 169patients,
92 % were symptomatic. The remaining patients had complaints originating from additional symptomatic ICA dissection. Neck pain and/or headache, predominantly reported on the affected side, were present in 84% of all
cases and in 88 % of patients with stroke. Vertigo is beside
head and neck pain, the most prominent sign in VA dissection with an incidence of 57 % (Saeed et al. 2000).
Cerebral infarction occurred in 67 % and a transient ischemic attack (TIA) in 10%. Subarachnoid haemorrhage
(SAH) was a rare event, occurring in 2 % of cases only
(Arnold et al. 2006a). Compared with ICA dissections,
pain seems to be less severe and more easily mistaken to
be musculoskeletal in origin (Silbert et al. 1995).
Therapeutic options for VA and ICA dissections are similar. Generally, initial intravenous heparinization followed
by 3–6 months of oral anticoagulation is recommended.
The underlying rationale is the prevention of secondary
embolic events as the majority of infarcts caused by dissection are of embolic origin (see also Case 11, p.183). The
risk of developing hemodynamic ischemic events is usually negligible because of the anatomic characteristics of
the posterior circulation (collateralization pathways, e. g.,
via the contralateral VA). Anticoagulation is contraindicated if the dissection extends into the intracranial compartment or if an SAH has occurred. Vessel restitution has
been reported in up to 71 % of cases (Bartels 1996). VA
dissecting aneurysms regress more frequently than ICA
dissecting aneurysms (Touzé et al. 2001).
Angiologic and Anatomic Aspects
Most spontaneous VA dissections are of extracranial location. The VA is fixed where its originates from the subclavian artery (SA), its passage through the spinal transverse
foramen, and at its entry through the dura mater. The
mobile segments in between, and in particular the transitional segments between mobile and fixed parts, are considered particularly prone to injury. Data on the precise
anatomic localization of VA dissections are contradictory.
This may in part be explained by the different ways used to
define the site of involvement. The beginning of the vessel
injury rather than the maximal or distal extension of the
hematoma should be considered as the site of dissection.
Applying this definition in 195 dissections, DSA or MRI
analysis has shown VA dissections of 20 %, 35 %, and 34 %
within the V1, V2, and V3 segments, respectively (Arnold
et al. 2006a). Extracranial VA dissections may extend into
the intracranial segments (Ansonand Crowell1991, Caplan
et al. 1988) and a small proportion of VA dissections arise
only intracranially. In the above cited study by Arnold and
coworkers, 79 % of VA dissections were extracranial, 10 %
extended into the intracranial VA, and only 11 % were
exclusively of intracranial location (Arnold et al. 2006a).
Extracranial duplex ultrasound is particularly sensitive in
localizing VA dissections within the entry zone into the
transverse foramen (C6). In this location, Bartels and coworkers (1996) were able to identify VA dissections in 11 of
26 dissections(42 %), characterized by an increase in vessel
diameter.
The most frequently observed VA pathology in dissection, however, is stenosis (56 %), followed by occlusion
(38 %) and dissecting aneurysm with stenosis (6 %) (Arnold
et al. 2006a). Comparable data were reported in a smaller
study with 42 % stenoses, 47 % occlusions and 12 % normal
findingsusingDSA,CTA,orMRA(Dziewasetal.2003).A
similar distribution pattern has been found in ICA dissection (Dziewas et al. 2003, Pelkonen et al. 2003).
Like in ICA dissections an involvement of the VA can
noninvasively be diagnosed by ultrasound, MRI, and CTA
techniques while conventional DSA has lost most of its
importance. As the VA is, at least in young subjects, well
accessible along most of its extracranial course, sonographic diagnosis should be attempted to search for direct
morphologic criteria. Typical findings are an irregular
stenosis, a thickened hypo- or isoechogenic vessel wall—
indicating the intramural hematoma, a double lumen, a
Degree of Neurosonologic Difficulty: Medium
Case 19 Vertebral Artery Dissection with Distal Occlusion
250
localvesseldistentionand/oradissectinganeurysm(Bartels 1996, Lu et al. 2000, Touboul et al. 1988). In young
patients as in our case, the examination of the VAs is not a
major concern. Therefore B-mode sonography was able to
reveal a hypoechogenic zone within the V2-VA segment,
probably corresponding to the mural hematoma. However, in the elderly and in patients with a large neck
circumferenceB-modeimagingqualitymaynotbesuffi-
cient to directly detect the dissection-related vessel wall
changes. In these cases, indirect hemodynamic signs may
be of help as they are indicative of stenosis or occlusion.
Increased or decreased flow velocities may be found depending of the length and degree of lumen narrowing. In
distalocclusion, high resistance flowsignals are seen in the
Degree of Neurosonologic Difficulty: Medium
proximal vessel segments as demonstrated in our case.
However, indirect hemodynamic criteria do not help in
distinguishing between occlusion caused by dissection,
embolism, or atherothrombosis. Also, VA hypoplasia and
anatomic variations might lead to difficulties in interpre-
tation of ultrasound findings. Analysis of the V2-VA vessel
diameter and blood flow may be of help. In hypoplasia, at
least a small diastolic flow should be preserved. In case of a
normal VA diameter the observed V2-VA flow alterations
depend on the location of the VA occlusion. ExtracranialV3
occlusion or intracranial V4 occlusion proximal to the PICA
origin will, as in our case, result in a distinct high resistance
flow signal without a diastolic flow component. Even a
“stump” signal may be seen if neck muscles collaterals
aremissing.Inthistypeofocclusion,retrogradefillingof
the distal V4-VA segment, ensuring blood flow into the
PICA, might be observed. A V4-VA occlusion, distal of the
PICA origin might result in normal V2-VA signals or only
mildly reduced diastolic flow velocities (see also Chapter 5,
“Intracranial Pathology,” p. 94). As V2-VA insonation alone
carries the risk of missing a distal V4-VA occlusion or highgrade stenosis, complete insonation of all VA segments
including the intracranial V4-VA segments should be performed, whenever pathology in the posterior circulation is
suspected. There have not been any large extensive studies
evaluating and comparing the importance of the above
dissection criteria. Considering both direct and indirect
signs, the reported sensitivity of ultrasound to detect VA
dissection ranges from 66 % to 100 % (Auer et al. 1998,
Bartels and Flugel 1996, de Bray et al. 1997, Pugliese et al.
2007).
The value of neuroradiologic methods has already been
discussed in relation to ICA dissections (see also Case 11,
p.183). In VA dissection, the intramural hematoma verification with MRI may be more difficult compared with ICA
dissection as the vessel diameter is smaller and the VA
often follows a more tortuous course, particularly within
the V3-VA segment. Arnold and coworkers report a success
rate of 91% (Arnold et al. 2006a). In our case, a mural
hematoma could not be visualized. The reason for this is
probably the time-dependent change in MRI blood sensitivity. Within the first days, the hematoma often appears
isointense to the surrounding body tissue, especially in the
T1-weighted sequences. From day 3 up to 2 months, a
distinct increase in the signal can be seen which subsequently fades and disappears over a period of approximately 6 months (Paciaroni et al. 2005). Early MRI, in our
case performed on day 2, might therefore fail to detect the
hematoma and, if applicable, a repeated scan might have
to be considered.
TOF MRA alone is not suitable in detecting VA dissection.
The reported sensitivity in a very small group of five VA
dissections was 20 %; the specificity was 100 % (Levy et al.
1994). With regard to multislice CTA, a retrospective study
in 17 patients with VA dissection and 17 controls using DSA
as reference reported a sensitivity, specificity, and positive
and negative predictive values of 100 %, 98 %, 95 %, and
100 %, respectively (Chen et al. 2004b). These excellent
results were recently confirmed by a second study in 15
patients yielding respective values of 100 %, 95 %, 93.7 %,
and 100 % (Pugliese et al. 2007). A comparison of duplex
ultrasound with CTA by the same group yielded values of
66 %, 60 %, 55.5 %, and 70.5 %, respectively.
Case 20
Internal Carotid Artery Dissection with Fast Recanalization
251
Clinical Presentation
A 56-year-old man presented with progressive paresis of
his left arm. Three days prior to presentation, he had
experienced some pain on the right side of his neck and
headaches while doing exercise in a gym for the first time.
The following day, he observed clumsiness of his left hand
and drooping of his right eyelid. The left-sided paresis
continued to progress, at which stage he presented to
our emergency department. The patient had no known
vascular risk factors. The neurologic examination revealed
a mild left-sided sensorimotor hemiparesis and Horner
syndrome on the right side (National Institute of Health
Stroke Scale [NIHSS] score 3).
Initial Neuroradiologic Findings
Cranial computed tomography (CCT) on the day of admission revealed multiple hypodensities in the right middle
cerebral artery (MCA) territory. Magnetic resonance
imaging (MRI) confirmed multiple ischemic lesions within
the internal border zone region of the right hemisphere.
Axial images demonstrated a reduced signal void in the
right carotid siphon. Time-of-flight (TOF) magnetic resonance angiography (MRA) depicted an absent signal of the
right distal internal carotid artery (ICA) and a bilateral
partial fetal-type posterior cerebral artery (PCA) origin
(Figs. B20.1–B20.3).
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B-mode imaging was normal. There were no atherosclerotic changes and no signs of proximal ICA dissection.
Doppler spectrum analysis showed a high pulsatility in
the right common carotid artery (CCA) and a high-resistance flow signal in the right ICA with a low and short
systolic flow and completely absent diastolic flow component, indicative of either near occlusion or occlusion of the
ICA below of the origin of the ophthalmic artery (OA).
External carotid artery (ECA) Doppler spectra were normal
(Figs. B20.4–B20.7).
Transcranial Duplex Sonography
The right M1-MCA segment presented a marked poststenotic flow pattern. The A1-ACA segment yielded a retrograde flow, also with severe poststenotic alterations. The
ACoA was not visualized. Elevated flow velocities were
seen in the right P1-PCA segment (125/69cm/s), here
with an obviously turbulent flow pattern, and in the left
A1-ACA segment (150/75cm/s), both indicative of collateral flow to the right anterior circulation via the anterior
(ACoA) and posterior (PCoA) communicating arteries. The
left MCA and PCA, in addition to the distal right P2-PCA
segment, demonstrated normal flow. No flow was detected in the OA on the right side. The flow signal of the
left OA was normal (Figs. B20.8–B20.13).
Suspected Diagnosis
Right internal border zone infarction (BZI) caused by ICA
dissection and secondary ICA occlusion.
Questions to Answer by Ultrasound Techniques
• Was there evidence of dissection?
• Was there a real occlusion or high-grade stenosis of the
ICA?
• If so, what were the intracranial collateral pathways?
Evaluation of Collateral Function
Cerebrovascular Reactivity Testing
Intravenous administration of 1 g acetazolamide during
continuous transcranial Doppler (TCD) monitoring of
both M1-MCA segments revealed a 60.6 % increase in
flowvelocityontheleftanda1.6%increaseinflowvelocity on the right side (Fig.B20.14)(seealsoChapter3,
“Parameters of Cerebral Hemodynamics,” p. 60).
Ultrasound Delay Testing
After intravenous administration of a 3-mL echo-contrast
bolus (Levovist, 300 mg/dL) and continuous monitoring of
both M1-MCA Doppler spectra, a right-sided, 1-second
Case 20 Internal Carotid Artery Dissection with Fast Recanalization
252
delay of bolus arrival was observed (Fig. B20.15)(seealso
Chapter 3, “Parameters of Cerebral Hemodynamics,” p.60).
Clinical Course (1)
Conclusion
Suspected right distal ICA dissection with near occlusion or
occlusion proximal to the OA origin. Exhausted CVR and
insufficient collateral pathways supplying the right MCA
territory via the ACoA and the ipsilateral PCoA
Conventional Angiography
Digital subtraction angiography (DSA) demonstrated a
Degree of Neurosonologic Difficulty: Medium
long, segmental irregularity in the caliber of the right
ICA. A cone-shaped high-grade stenosis started 5 cm above
the carotid bifurcation and extended up to the vertical
segment of the petrous C6-ICA segment. Only residual
and delayed contrast filling was seen in the distal ICA.
Collateralization mainly occurred via the ACoA and partially via a hypoplastic right P1-PCA segment providing
retrograde blood flow into the right MCA via the fetaltype PCA and orthograde blood flow into the distal PCA
segments. Filling of the right MCA territory was delayed.
These findingswere consistentwith a near occlusion of the
right ICA due to vessel wall dissection (Figs. B20.16–
B20.21).
Figure B20.22shows a schematic drawing of the extra- and
intracranial brain-supplying arteries of the patient.
Intravenous heparin, aiming for a twofold rise of partial
thromboplastin time (PPT) was started. TOF MRA 2 weeks
later demonstrated a normalized right ICA signal.
Follow-up Neurosonologic Findings (Day 20)
Extracranial Duplex Sonography
A normalized flow pattern was seen in the right CCA and
ICA compared with the contralateral side (Figs. B20.23–
B20.26).
Transcranial Duplex Sonography
TherightM1-MCAandA1-ACAaswellasthePCAsegmentsdemonstratednormalizedflowvelocitiesandpulsatility. A flow within the hypoplastic right P1-PCA segment was no longer detectable (Figs. B20.27–B20.32).
Conclusion
Flow normalization in all insonated vessels indicating a
rapid resolution of the right ICA dissection.
Fig. B20.1 MR T2-weighted image, axial plane. Multiple hyperintense signals within the right internal border zone, indicative of
hemodynamic infarction.
Fig. B20.2 MR T2-weighted image, axial plane. Absent flow void
within the right-sided cavernous ICA segment, suggestive of reduced or abolished intraluminal flow (arrow).
Clinical Course (2)
The patient was switched to oral anticoagulation with
phenprocoumon and was discharged with a mild leftsided hemiparesis. Anticoagulation was stopped 6 months
later. Until that time no further clinical events had occurred and the left hemiparesis had completely resolved.
Final Diagnosis
Right internal BZI after distal ICA dissection with subsequent near occlusion and initially insufficient collateral
blood flow via the ACoA and PCoA. Rapid vascular normalization within 3 weeks.
Final Diagnosis
Fig. B20.3 Intracranial 3D TOF MRA, axial MIP. Signal loss of theright
ICA indicating high-grade flow reduction or occlusion. Note the
bilateral fetal-type PCA (arrowheads). Both P1-PCA segments are
hardly visible.
253
Degree of Neurosonologic Difficulty: Medium
Fig. B20.4 Extracranial duplex, longitudinal plane. Normal left CCA
flow (flow velocity: 87/28 cm/s).
Fig. B20.6 Extracranial duplex, longitudinal plane. Normal flow signal in the left ICA (flow velocity: 79/40 cm/s).
Fig. B20.5 Extracranial duplex, longitudinal plane. High resistance
flow signal in the right CCA (peak-systolic flow velocity: 63 cm/s).
Fig. B20.7 Extracranial duplex, longitudinal plane. High-resistance
flow signal in the right ICA with a low and short systolic, and
completely absent diastolic flow component indicative of near occlusionorocclusionoftheICAbelowtheOAorigin.
Case 20 Internal Carotid Artery Dissection with Fast Recanalization
254
Degree of Neurosonologic Difficulty: Medium
Fig. B20.8 TCCS (transtemporal approach), left-sided insonation,
midbrain plane. Normal left M1-MCA flow (flow velocity: 69/
31 cm/s) Note the prominent lef t PCoA with a blue-coded signal
indicating flow toward the P2-PCA (arrow).
Fig. B20.10 TCCS (transtemporal approach), left-sided insonation.
Increased nonturbulent flow in the left A1-ACA, indicative of collateral flow (flow velocity: 150/75 cm/s).
Fig. B20.9 TCCS (transtemporal approach), right-sided insonation.
Poststenotic flow pattern in the right M1-MCA (flow velocity: 54/
38 cm/s).
Fig. B20.11 TCCS (transtemporalapproach), right-sidedinsonation.
Retrograde, poststenotic flow pattern in the right A1-ACA (flow
velocity: 45/35 cm/s).
Fig. B20.12 TCCS (transtemporal approach), left-sided insonation.
Normal flow in the left P1-PCA (flow velocity: 50/20 cm/s). Note
again the prominent left blue-coded PCoA with flow toward the P2PCA indicating a partial fetal-type PCA.
Fig. B20.13 TCCS (transtemporalapproach), right-sidedinsonation.
Turbulent signal and increased flow velocity in the right P1-PCA (flow
velocity: 125/69 cm/s) indicating a hypoplastic vessel (functional
stenosis). Note the red-coded right-sided PCoA with a flow direction
toward the ICA (arrow).
Final Diagnosis
Fig. B20.14 Acetazolamide infusion test, bilateral TCD monitoring of M1-MCA flow. Exhausted CVR in the right MCA. Note a marked
difference between the right and left sides,
with an increase in flow velocity of 60.6 % on
the left and of 1.6 % on the right side after
15 minutes.
Fig. B20.15 Echo contrast delay test, bilateral
TCD monitoring of M1-MCA flow, revealing a
delay of 1 s on the right side. Top: right MCA,
bottom: left MCA. Note the signal enhancement of the Doppler spectrum caused by the
inflow of the intravenous Levovist echo-contrast bolus at approximately 12 seconds on the
left (black arrow) and at 13 seconds on the
right side (white arrow).
255
Degree of Neurosonologic Difficulty: Medium