AJR 2005; 184:S7-S9
© American Roentgen Ray Society
Determination and Follow-Up of Striolenticular Vasodilatation and Hyperemia After Acute Embolic Stroke: Demonstration on MR Angiography
K. Wolfgang Neff1,
Dietmar Dinter1,
Andreas Schwartz2 and
Christoph Düber1
1 Department of Clinical Radiology, Universitätsklinikum Mannheim,
University of Heidelberg, Theodor Kutzer Ufer 1-3, 68167 Mannheim,
Germany.
2 Department of Neurology, Universitätsklinikum Mannheim, University of
Heidelberg, Mannheim, Germany.
Received April 13, 2004;
accepted after revision June 14, 2004.
Address correspondence to K. W. Neff
(wolfgang.neff{at}rad.ma.uni-heidelberg.de).
Introduction
Transient hypoperfusion of blood vessels disturbs vessel
autoregulation, inducing vasodilatation and hyperemia after early
recanalization. This phenomenon, detected using 3D time-of-flight (TOF) MR
angiography, and its time course, have not been reported in the literature. It
has been observed by conventional (X-ray) angiography and reported in patients
with acute stroke in a small number of cases
[1,
2]. In addition, MRI
[3] and CT
[4,
5] have been used to
investigate vascular hyperemia after stroke, increased parenchymal blood
volume after recanalization as a result of increased flow into salvageable
tissue, and blush phenomenon, but none of these less invasive techniques can
demonstrate the actual dilatated and hyperemic vessels. We present a case in
which MR angiography demonstrated lenticulostriate vessel dilatation and
describe the serial time course of this hyperemia phenomenon after acute
stroke.
Case Report
An 18-year-old woman with a right-sided headache and acute left-sided
sensorimotor hemiparesis with initial hemiplegia of the left arm was admitted
to the hospital. Neurologic examination revealed a left-sided sensorimotor
hemiparesis, predominantly in the arm and face, with positive left pyramidal
signs. Initial cranial CT 6 hr after the onset of symptoms showed no
abnormalities. The first MR examination (1.5 T MR-unit, Magnetom Vision,
Siemens Medical Solutions) 15 hr after the onset of symptoms revealed cerebral
infarction with hyperintense lesions in T2-weighted images in the head of the
caudate nucleus and right lentiform nucleus and a small cortical infarction of
the right middle cerebral artery (MCA) territory
(Fig. 1A).
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Fig. 1A. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm.
Initial axial T2-weighted turbo spin-echo MR image obtained 15 hrs after
symptom onset shows a typical embolic pattern of infarction with hyperintense
lesions in right lentiform nucleus, right head of caudate nucleus, and
cortical, parieto-temporal region of right middle cerebral artery (MCA)
territory.
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This observation was underlined by 3D TOF MR angiography (magnetization
transfer saturation [MTS] tilted optimized nonsaturating excitation [TONE];
TR/TE, 38/7; flip angle, 20°; field of view, 200 cm; matrix, 256 x
256; slab thickness, 64 cm; number of excitations, 1; partitions, 64) (Figs.
1B and
1C), detecting a probable
stenosis in the distal M1 segment of the right MCA and early vasodilatation
with hyperemia of the first lateral group of right striolenticular branches
extending into the infarction area as a sign of acute disturbance of vessel
autoregulation (Fig. 1C). The
patient was treated with full-dose IV heparin therapy and oral nimodipine (60
mg twice a day). Fibrinolysis was not performed because the time between
admission to the hospital and symptom onset was 6 hr and the clinical symptoms
were beginning to subside. The patient's headache was already gone and paresis
of the left arm was still observed but was mild, persisting for 72 hr.
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Fig. 1B. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm. Axial
initial magnetization transfer saturation (MTS) tilted optimized nonsaturating
excitation (TONE) time-of-flight (TOF) MR angiography
maximum-intensity-projection (MIP) reconstruction (matrix 256 x 256)
demonstrates moderate, probable stenosis of distal M1 segment of right MCA and
vasodilatation with hyperemia of right striolenticular branches extending into
the infarction area of the right lentiform nucleus (arrow).
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Fig. 1C. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm.
Initial MTS TONE TOF MR angiography MIP reconstruction (coronal projection,
matrix 256 x 256) demonstrates moderate, probable stenosis of the distal M1
segment of right MCA and vasodilatation with hyperemia of right
striolenticular branches extending into the infarction area of right lentiform
nucleus (arrow).
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Transcranial Doppler (TCD) examination confirmed a stenosis in the distal
M1 segment of the right MCA with peak blood flow velocities up to 200 cm/sec
at a depth of 50-55 mm, which corresponded exactly to the MR angiography
findings. No further abnormalities were detected on sonography of the intraand
extracranial arteries. TCD monitoring of the right MCA revealed spontaneous
microembolization distal to the stenosis in the M1 segment. No
microembolization was found in other vessels of the circle of Willis. The
distal M1 stenosis was detectable in TCD for 2 days; the increased blood flow
velocities decreased to normal values of about 110 cm/sec. Transesophageal
echocardiography revealed an open foramen ovale with a spontaneous
right-to-left atrial shunt, particularly under Valsalva's maneuver. No further
source of embolus was found. ECG and cerebrospinal fluid findings were normal.
Routine laboratory values were unremarkable, except for an elevated
cholesterol of 380 mg/dL.
At 3D TOF MR angiography follow-up after 1 week (matrix 256 x 512,
Figs. 1D and
1E), the striolenticular
vasoparalysis with vasodilatation and hyperemia were unchanged and the
probable stenosis of the right MCA had disappeared because of recanalization.
The pattern of infarction in the right MCA territory with its typical
evolution had not changed on the MRI study. Follow-up TCD and duplex system
examinations confirmed the MR angiography findings of recanalization of the
right MCA. On TCD monitoring, microembolization was no longer detectable in
the right MCA. After two weeks of fulldose IV heparin therapy, anticoagulation
with coumarin was initiated for 3 months.
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Fig. 1D. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm.
High-resolution axial MTS TONE TOF MR angiography (MIP reconstruction, matrix
256 x 512) follow-up 1 week after onset of symptoms shows probable
recanalization of distal M1 segment of right MCA and persisting vasodilatation
with hyperemia of right striolenticular branches (arrow).
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Fig. 1E. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm.
High-resolution MTS TONE TOF MR angiography MIP reconstruction (coronal
projection, matrix 256 x 512) follow-up 1 week after symptom onset shows
probable recanalization of distal M1 segment of right MCA and persisting
vasodilatation with hyperemia of right striolenticular branches
(arrow).
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MR angiography follow-up after 2 weeks, 3 weeks after the onset of the
symptoms, confirmed the complete recanalization of the right MCA, but the
striolenticular vasodilatation and hyperemia had disappeared (Figs.
1F and
1G). Cerebral ischemic regions
showed the typical time course in MRI. The patient was free of symptoms.
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Fig. 1F. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm. In
high-resolution MTS TONE TOF MR angiography (axial MIP reconstruction, matrix
256 x 512) follow-up 2 weeks later, 3 weeks after onset of symptoms,
vasodilatation with hyperemia of right striolenticular branches was no longer
detectable.
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Fig. 1G. —18-year-old woman with right-sided headache and acute
left-sided sensorimotor hemiparesis with initial hemiplegia of left arm. In
high-resolution MTS TONE TOF MR angiography (coronal MIP reconstruction,
matrix 256 x 512) follow-up 2 weeks later, 3 weeks after symptom onset,
vasodilatation with hyperemia of right striolenticular branches was no longer
detectable.
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Discussion
The most specific finding in the acute phase of cerebral ischemia is vessel
stenosis and occlusion, seen in about 70% of all angiograms performed within
the first few hours after cerebral infarction
[6]. Collateral filling,
hyperemia, or vascular blush in the ischemic region and penumbra (luxury
perfusion) are angiographic manifestations that can be identified in 15-25% of
cases, whereas the presence of local hematomas in ischemic regions, including
petechial hematomas, can be seen after intraarterial thrombolysis in a larger
number of acute stroke patients (50-75%)
[3-5].
The blood volume, which initially decreases in cerebral ischemia, increases in
the subacute stage, reflecting reperfusion hyperemia, and decreases again in
the chronic stage. The time interval between onset of stroke and CT or MRI
examination must be considered to correctly interpret blood volume data in
cerebral infarction at various stages
[7]. With MR angiography,
vascular occlusion or stenosis can be demonstrated in many patients, but spin
saturation reduces the sensitivity for small or distal vascular lesions.
Although inferior vessels can be displayed, with increased spatial resolution,
MR angiography can also show most proximal lesions (first- and proximal
second-order segments) visible on selective intraarterial angiography
[8]. Modern dedicated
high-spatial-resolution MR angiography has been shown to offer good image
quality also for vessel stenosis or occlusion (e.g., in evaluating cerebral
aneurysms [8]), and can map
intracranial vessels up to second- and third-order segments. However, more
distant lesions have to be diagnostically validated by conventional
angiography.
Hypoperfusion and reactive hyperemia or hyperperfusion are the two major
postischemic circulatory disturbances in the pathophysiology of an ischemic
lesion. The reactive hyperemia or hyperperfusion in combination with
vasodilatation, known as vasoparalysis, promptly follows early recanalization
after occlusion of a brain-supplying cerebral artery. Until now, the detection
of those alterations has been restricted to selective intraarterial
angiography and CT or MRI
[1-5].
In the present case, the serial time course of vasodilatation and hyperemia of
the striolenticular branches could be detected and demonstrated over three
weeks after thromboembolic ischemia of the basal ganglia using MR
angiography.
At the early stage of onset, a well-defined pattern of infarction with
lesions in the right lentiform nucleus, head of the caudate nucleus, and a
small cortical infarction of the right MCA in the temporoparietal territory
could be confirmed by MRI. This indicates a focal stenotic thromboembolic
mechanism in the right MCA, and the pattern of MRI lesions suggests a
transient proximal MCA occlusion with persistent damage in the striolenticular
territory but good collateral supply of the cortex until recanalization.
Initial MR angiography was able to detect a residual circumscript stenosis of
the distal M1 segment of the right MCA. The stenosis was confirmed by TCD and
transcranial duplex-system findings. Embolus was established as a possible
source after microemboli were detected distal to the stenosis in the right
MCA. Follow-up of spontaneous lysis of embolic thrombus, (stenosing the MCA
main trunk and occluding the striolenticular orifices) within a few days after
onset of acute stroke and recanalization of the M1 segment of the right MCA
was shown by TCD, TCD monitoring, and MR angiography.
The presentation of striolenticular hyperemia and its evolution are well
known in conventional angiograms
[1]. In the present case, all
hyperemia and vasodilatation changes were demonstrated and the serial time
course of this hyperemia phenomenon could be described by 3D TOF MR
angiography, including the visualization of third-order vessels with diameters
normally 300-500 µm.
References
- Kawase T, Mizukami M, Tazawa T, Araki G. The significance of
lenticulostriate arteries in transient ischemic attack: neuroradiological and
regional cerebral blood flow studies. No To Shinkei1979; 31:1033
-1040[Medline]
- Olsen TS, Skriver EB, Herning M. Radiologic manifestations of focal
cerebral hyperemia in acute stroke. Acta Radiol1991; 32:100
-104[Medline]
- Greer DM, Koroshetz WJ, Cullen S, Gonzales RG, Lev MH. Magnetic
resonance imaging improves detection of intracerebral hemorrhage over computed
tomography after intra-arterial thrombolysis. Stroke2004; 35:491
-495[Abstract/Free Full Text]
- Mericle RA, Lopes DK, Fronckowiak MD, Wakhloo AK, Guterman LR,
Hopkins LN. A grading scale to predict outcomes after intra-arterial
thrombolysis for stroke complicated by contrast extravasation.
Neurosurgery2000; 46:1307
-1314[Medline]
- Nakano S, Iseda T, Kawano H, Yoneyama T, Ikeda T, Wakisaka S.
Parenchymal hyperdensity on computed tomography after intra-arterial
reperfusion therapy for acute middle cerebral artery occlusion.
Stroke 2001;32:2042
-2048[Abstract/Free Full Text]
- Horowitz SH, Zito JL, Donnarumma R, Patel M, Alvir J. Computed
tomographic-angiographic findings within the first five hours of cerebral
infarction. Stroke1991; 22:1245
-1253[Abstract/Free Full Text]
- Kim JH, Shin T, Chung JD, et al. Temporal pattern of blood volume
change in cerebral infarction: evaluation with dynamic contrast-enhanced
T2*-weighted MR imaging. AJR1998; 170:765
-770[Abstract/Free Full Text]
- Barboriak DP, Provenzale JM. MR arteriography of intracranial
circulation. AJR1998; 171:1469
-1478[Free Full Text]
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Introduction
Case Report
