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Cerebrovascular abnormalities in pediatric stroke Assessment using parenchymal and angiographic magnetic resonance imaging.

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Cerebrovascular Abnormahties in Pediatric
Stroke: Assessment Using Parenchymal and
Angiographc Magnetic Resonance Imaging
Max Wiznitzer, MD,'? and Thomas J. Masaryk, MDSS
Three-dimensional (volume) magnetic resonance angiography is a noninvasive technique that images the intracranial
and cervical arterial vasculature without contrast agents. Twenty-four children with strokes had combined parenchymal magnetic resonance imaging and magnetic resonance angiography 1 day to 4 years after acute presentation. Eight
had had prior intra-arterial angiography. Eighteen magnetic resonance angiographic studies showed arterial stenosis
or occlusion in the vascular distribution of magnetic resonance image-defined brain infarction and, in 7 children, in the
same location as previously defined abnormalities on intra-arterial angiography. One child had a normal intra-arterial
angiogram and magnetic resonance angiogram. The other 5 children with normal magnetic resonance angiographic
studies included 3 with presumed embolic disease, 1 with meningitis, and 1 with Crohn's disease-related vasculitis.
Collateral flow patterns could be determined in 4 children. Artifact presenting as filling defects in vessels was present
in 10 studies, but did not interfere with interpretation of 8 studies. Combined magnetic resonance imaginglmagnetic
resonance angiography provides a screening technique to evaluate noninvasively brain parenchyma and vasculature
in children with suspected large-vessel abnormalities, allowing selection for intra-arterial angiography and serial
monitoring of vascular abnormalities over time and during therapeutic intervention.
Wiznitzer M, Masaryk TJ. Cerebrovascular abnormalities in pediatric stroke:
assessment using parenchymal and angiographic magnetic resonance
imaging. Ann Neurol 1991;29.585-589
Strokes in children have an annual incidence of 2.52
per 100,000, with 25% being ischemic events. Sequelae are common, including hemiparesis, visual field
deficits, epilepsy, and learning disabilities 111. Computed tomographic (CT) scan and magnetic resonance
imaging (MRI) can identify areas of parenchymal injury
but cannot assess definitively the status of the cerebral
vasculature [2, 31. Doppler ultrasonography can demonstrate changes in vascular flow patterns but might
not always be a reliable screening technique 14, 51.
The assessment of cerebrovascular abnormalities has
required intra-arterial angiography with its attendant
risks [GI. A new technique that uses magnetic resonance principles to image noninvasively the large cervical and intracranial blood vessels without the use of
contrast media, known as three-dimensional (volume)
magnetic resonance angiography (MRA), is now available 171. We report our initial assessment of the applicability of MRA in the evaluation of the cervical and
intracranial vasculature in children with cerebral infarctlon compared with the location of the brain parenchymal lesion and with results of intra-arterial angiography.
From the Departments of *Pediatrics and $Radiology, Case Western
Reserve University, tDivision of Pediatric Neurology, Rainbow Babies and Chlldrens Hospital, and IUniversity Hospitals of Cleveland,
OH.
Methods
Subjects for magnetic resonance studies were chosen from
two populations. Fourteen children with known cerebral in-
farction were referred for MRA studies. Ten additional children, with acute neurological dysfunction,were prospectively
seen at Rainbow Babies and Childrens Hospital (Cleveland,
OH) between January 1988 and March 1990. All children
had CT-proved or MRI-proved intracranial parenchymal infarctions in a vascular distribution. Eight children had intraarterial angiography to identify cerebrovascularabnormalities
within 1 month of onset of neurological dysfuncuon. Six children with sickle cell anemia have been previously reported
[8}. Informed consent for the magnetic resonance studies
was obtained from a parent or legal guardian.
Magnetic resonance studies were done on a Magnetom
1.5-T system (Siemens, Iselin, NJ) with a gradient capability
of 10 mTlm and using a linearly polarized, transmit-andreceive mode head coil. Parenchymal studies were performed
with T2-weighted axial and T1-weighted sagittal or coronal
spin echo sequences, or both. MRA was always done in conjunction with the parenchymal MRI study and used time-offlight sequences designed to promote flow-related enhancement. Cervical studies consisted of a three-dimensional
Fourier transform FLASH (fast low angle shot) sequence with
flip angle equal to 30 degrees, repetition time (TR)/echo
Received Aug 24, 1990, and in revised form Nov 26. Accepted for
publication Dec 3, 1990.
Address correspondence to Dr Wiznitzer, Rainbow Babies and Childrens Hospital, 2101 Adelben Road, Cleveland, OH 44106.
Copyright 0 1991 by the American Neurological Association
585
Table 1. Sttldy Poptllation and Findings
Etiology
Neurological Exam
MRIiInfarction
MRA
1
2
Prenatal
Prenatal
R Hemiparesis
R Hemiparesis
0 - L Distal MCA
0 - L Proximal MCA
3
Prenatal
R Hemiparesis
4
Prenatal
L Hemiparesis
L Temporaliparietal
L MCA Cortical and
subcortical
L Frontalltemporali
parietal
R Frontalitemporal
5
Hypoxic-ischemic
encephalopathy
Crohn's disease
Traumatic dissection
R Hemiparesis
L Temporaliparietal
R Hemiparesis
Bil basal ganglia
Bil cerebellum,
R Occipital
Bil cerebellum
L Pons
Bil cerebellum, L
internal capsule
L Frontal
Bilateral DWM
Patient No.
6
78
Arterial dissection
9"
Migraine
L Hemiparesis
Ataxia
R Hemiparesis
Ataxia
Ataxialtremor
10"
11"
Sickle cell anemia
Sickle cell anemia
12a
13
Sickle cell anemia
Sickle cell anemia
14
Sickle cell anemia
L Hemiparesis
15
17
Sickle cell anemia
Cardiac catheterization
Cardiac surgery
18
Cardiac surgery
R Hemiparesis
L Hemiparesis
L Hemiparesis and
hemiparesthesia
L Hemiparesis
16
R Hemiparesis
Transient aphasia and
R hemiparesis
Transient hemiparesis
R Hemiparesis and
diparesis
19
20
Bacterial endocarditis
Lupus erythematosus
R Hemiparesis
R Hemiparesis
21
22"
Bacterial meningitis
Moya-Moya disease
R Hemiparesis
R Hemiparesis
23"
24
Unknown
Unknown
L Hemiparesis
R Hemiparesis
Patent L MCA and absent
branches
Patent R MCA and decreased
branches
0 - L Proximal MCA
WNL
0 - L Vertebral
Hypoplastic R vertebral
0-Basilar and Bil proximal PCA
L Hypoplastic vertebral
Narrow Bil PCA
0 - L ICA
S-Bil ICA
S-Bi1 ICA
0 - L ICA
Bilateral DWM
L Frontal/parientall
temporal,
bilateral DWM
R Frontallparietali
temporal
Bilateral DWM
R Parietal
R Basal ganglia
S-Bil ICA and proximal MCA
WNL
0 - R Distal ICA-MCA
R MCA Cortical and
WNL
subcortical
L Frontal
L Frontalltemporali
parietal
L Frontallparietal
L Frontal and Bil
DWM
R Hemiparesis
L Basal ganglia
0 - R ICA
WNL
0 - L Proximal MCA
WNL
S-BiI Distal ICAIMCA; 0 - L
MCA
WNL
0 - L Proximal MCA
"Inrra-arterial angiography done
MRI = parenchymal magnetic resonance imagiag; MRA = magnetic resonance angiography;R = right; L = left; MCA = middle cerebral artery; ICA = internal
carotid artery; PCA = posterior cerebral artery; DWM = deep white marrer infarction; 0 = occlusion; S = scenosis; WNL = normal; Bil = bilateral.
time (TEj equal to 40 to 50 mseci7 to 8 msec, and axial
excitation of a coronal volume containing 64 1.5-mm slices.
Intracranial MRA studies were done with a threedimensional FISP (fast imaging with steady precession) sequence with TRlTE equal to 40 to 50 msecl7 to 12 msec, a
15-degree flip angle, and an axial volume with 32 to 128
slices of 0.8 to 1.3-mm thickness. Examination time for either
study was 7 to 15 minutes. Data were reconstructed for postprocessing analysis on a Vax 750 (Digital Equipment, Marlboro, MA). Details of the procedure have been previously
described {S- 103. Magnetic resonance studies were interpreted by radiologists who had no knowledge of the child's clinical history or other neuroimaging tests.
Results
Demographic, MRJ, and MRA findings are listed in
the Table. Patients 1 to 14 were the retrospective
586 Annals of Neurology
Vol 29 No 6 June 1991
group. The rest were studied prospectively. The mean
age of all children at the time of the magnetic resonance studies was 7.0 years, with studies done at an
average age of 8.0 years for the retrospective and 5.5
years for the prospective groups. Magnetic resonance
studies were performed at a mean interval of 3.5 years
after stroke occurrence in the retrospective group and
within 1 month of presentation in the prospective
group. Eight children had presumed thrombotic vascular occlusion, whereas emboli were the causative factor
in 8. Also, the 2 children with arterial dissection had
vascular occlusion with parenchymal lesions that could
have been secondary to resultant thrombotic emboli.
All children had intracranial M U studies, which adequately visualized the petrous, cavernous, and supraclinoid internal carotid artery, the proximal anterior
A
B
Fig 1. Patient 24. This 2-year-old boy presented with sadden
onset of right hemiparesis. (A) T2-weighted magnetic resonance
imaging showed high-intensity signal in the lefd basal ganglia
(consistent with hemorrhagic infarction seen on prior computed
tomographicscan). (B) Axial intracranial magnetic resonance
angiography demonstrated absence of blood flow beyond the origin of the left middle cerebral artery (large arrow) and collateral
blood flmv f m m posterior cerebral and leptomeningeal arteries
(small arrows).
cerebral artery, the middle cerebral artery and its primary Sylvian branches, and the distal vertebral and entire basilar arteries. Early MRA studies imaged the
proximal posterior cerebral artery, whereas later studies defined its course to the occipital region. Eleven
children had cervical M U studies with good definition
of the distal common carotid artery, proximal external
carotid artery, the internal carotid artery to the level
of the petrous ridge, and the vertebral artery to the
level of the foramen magnum. Eighteen MRA studies
showed abnormalities in the expected vascular distribution of parenchymal lesions (Figs 1, 2). Normal MRA
studies were found in 3 children with presumed embolic disease, 1 with meningitis, 1 with small-vessel
disease due to Crohn’s disease, and 1 with a normal
angiogram.
Eight children (Patients 7-12, 22, and 23) had intraarterial angiography at the time of stroke presentation.
MRA studies were done 1 to 4 years (average, 2.8
years) after the initial angiogram in 6 retrospective
children and within 1 month in 2 prospective children.
Large-vessel abnormalities on MRA were comparable
with those on intra-arterial angiography and, in Patient
12, suggested stenosis of the distal left internal carotid
artery that was confirmed on review of the initial intraarterial angiogram. Patient 5 had an intracranial ultrasound at age 2 days that showed loss of left middle
cerebral artery pulsations. MRA demonstrated occlusion of the proximal left middle cerebral artery and
associated left temporoparietal infarction at age 2 years.
Collateral flow patterns were imaged on MRA. Two
children with internal carotid artery occlusion (Patients
10 and 13) had flow signal in the ipsilateral posterior
communicating artery, suggesting flow from the posterior to anterior cerebral circulation, with evidence of
distal internal carotid artery and ipsilateral middle cerebral artery flow signal. Two children with posterior
circulation occlusions had flow signal in both posterior
communicating arteries with posterior cerebral artelry
flow partially (Patient 7) or wholly (Patient 8) dependent on these vessels (see Fig 2).
Filling defects in blood vessels as a result of flow
void artifact were noted in 10 children (42%). These
were located at the internal carotid siphon [9}, distal
internal carotid artery bifurcation [S], or knee of the
proximal middle cerebral artery [4]. Flow void in these
regions was bilateral in 9 children. Eight of these were
early studies with TE equal to 12 to 15 msec. Flow void
in these studies did not interfere with identification of
areas of vascular occlusion. In the other two studies,
repeat MRA using thinner (0.8 mm) slices eliminated
the artifact and allowed for adequate MRA interpretation.
Discussion
The definitive diagnosis of cerebrovascular abnormalities in pediatric vaso-occlusive stroke has required
Wiznitzer and Masaryk: Cerebrovascular Abnormalities in Pediatric Stroke
587
A
B
L
588 Annals of Neurology Vol 29 No 6 June 1991
intra-arterial angiography. This procedure is done in
children without an easily identifiable cause for stroke
or whose treatment is dependent on the presence or
absence of vascular lesions, such as the sickle hemoglobinopathy population { 11, 121. Complications include
the precipitation of transient or permanent focal neurological deficits, reaction to contrast media, and trauma
to the artery of access. Studies in the adult population
report 1% morbidity and 0.4% mortality for angiography [GI. General anesthesia with its attendant risks
is usually required for sedation. Preparation for angiography may require blood transfusion, which can be associated with anaphylactic and other immunological reactions and infection. These potential complications
might preclude the use of angiography by physician or
parent.
Alternative noninvasive procedures are avadable to
assess the cerebral vasculature. Absence of blood flow
signal in the internal carotid artery and proximal middle cerebral artery can be seen on brain parenchymal
MRI but usually requires confirmation by intra-arterial
angiography [31. Doppler ultrasonography can evaluate
changes in blood flow velocity in extracranial and intracranial cerebral vessels and is useful in the detection
of vascular occlusion or stenosis greater than 60%.
Limitations of ultrasound include the inability to identify mild intracranial stenosis, symmetrical vascular abnormalities, and portions of the vertebrobasilar circulation and distal middle cerebral arteries; possible
confusion in identification of intracranial vessels; difficulties in the establishment of an ultrasonic window in
5 to 15% of patients; and the absence of good anatomical definition [4, 53.
Our findings suggest that MRA is an acceptable
screening technique for large-vessel disease in the anterior and posterior cerebral circulations in children. In
our population, vascular abnormalities on MRA were
consistently located in the appropriate vascular distribution of parenchymal infarcts. MRA demonstrated
the same large cerebral vessel findings as intra-arterial
Fig 2. Patient 8. This 4-year-old boy developed ataxia and
nkht hemiparests over several hours. Magnetic resonance imaging scan showed bilateral cerebellar and left pontine infarction. (A) Intraarterial angiography was done after 2 week
and revealed complete occlusion of the distal basilar artery with
a pseuohaneuysm suggestive of arterial dissection (open arrow).
(B) Internal carotid artery injection showed blood supply t o the
posterior cwebral arteriu through the posterior communicating
arteries (closed arrow). (C) Lateral view of an intracranial
magnetic resonance angiogram done 2 years later demonstrated
persistent occlusion of the basilar artery (open arrow) with continued dependence of posterior cerebral artery blood supply on
flow from the internal carotid a r t w through the posterior communicating artey (closed arrow). I = internal carotid artey;
P = posterior cerebral artery.
angiography in all 8 patients studied by both methods.
Normal MRA studies were found in children with
strokes secondary to presumed va.ospasm, emboli, and
small-vessel disease. Emboli might not be identrfied on
MRA if they fragment after occlusion of a major cerebral vessel or involve smaller branches. In addition to
arterial and venous thrombotic occlusion, vaospasm
has been reported in meningitis-associated stroke and
is a temporary phenomenon with normal intra-arterial
angiogaphy after disease resolution { 131.
Limitations to this procedure exist. Imaging is restricted to the larger cerebral vessels because penetrating arteries are not visuahed. The field of view is
restricted to a volume slab that must be properly positioned for adequate definition of the vessels in question. With use of sequential two-dimensional slices or
multiple, thinner, three-dimensional slabs, the field of
view can be expanded. Turbulence and rapid changes
in vessel direction (such as the internal carotid siphon
and bifurcation) can produce flow void artifact that
simulates stenotic-occlusive lesions { 141. Use of thinner slices, examination of the individual slice acquisitions, and changes in acquisition parameters can usually
determine if artlfact or vascular disease is present. If
questionable areas of vascular narrowing persist, intraarterial angiography can then be used. Areas of very
slow flow, such as venous angiomas or dolichoectasia,
are poorly imaged by three-dimensional MRA without
the use of contrast media [lS}. In children with stroke,
this is not of significant concern. Slow flow can also
occur distal to severely stenotic regions, such as dissection or intimal hyperplasia in sickle cell anemia. In our
population, reconstitution of flow was apparent distal
to stenotic lesions in those with sickle cell anemia and
no flow was seen in those with arterial occlusion, both
findings confirmed by angiography. Further experience
with MRA is needed before definite conclusions about
the differentiation between severe stenosis and occlusion can be made.
In this study, collateral flow patterns can only be
inferred by the absence of alternative possibilities for
blood supply, such as in Patients 7, 8, 10, and 13.
Directionality of flow has been recently demonstrated
by using MRA. This method, known as selective MRA,
shows collateral flow patterns by eliminating flow signal
from selected blood vessels and noting if flow in contiguous regions is affected { lb].
MRA can be used as a screening procedure in children with vaso-occlusive disease and, with greater discretion, in those with suspected vascular stenosis. It is
noninvasive and requires no contrast media. Sedation,
if necessary, can be given orally or intramuscularly, and
does not require general anesthesia. Study time for
either cervical or intracranial vessels is 7 to 1 5 minutes
and can be appended to a brain parenchymal MRI scan.
In children with normal MRA studies who have susWiznitzer
pected intracranial large-vessel stenosis, embolic occlusion of smaller vessels, or small-vessel disease, further
investigation with intra-arterial angiography can be
done. Prior use of MRA will decrease the need for
intra-arterial angiography and its associated complications. MRA can be used to screen populations at higher
risk for stroke, including children with sickle hemoglobinopathy whose siblings have had a stroke, children
with collagen disorders, children with fibromuscular
dysplasia, and children with a history of craniocervical
radiation therapy. Another potential use is the monitoring of vascular effects of treatment protocols, such
as thrombolytic therapy for acute stroke, anticoagulation for progressive stroke, or chronic transfusion therapy in children with sickle cell anemia and prior stroke.
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and Masaryk: Cerebrovascular Abnormalities in Pediatric Stroke 589
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