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Middle Cerebral Artery Stenosis Is a Major Clinical Determinant in Striatocapsular Small, Deep Infarction
Oh Young Bang, MD;
Ji Hoe Heo, MD;
Jung Yeon Kim, MD;
Jae Hyun Park, MD;
Kyoon Huh, MD
Arch Neurol. 2002;59:259-263.
ABSTRACT
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Background The significance of the stenotic lesions of the middle cerebral artery
(MCA) in Asian patients with striatocapsular small, deep infarctions (SSDIs)
remains undetermined.
Objectives To investigate the frequency of stenotic lesions of the MCA in patients
with SSDIs and to evaluate clinical and radiological features in those same
patients.
Setting Acute stroke registry of a university hospital.
Patients and Methods One hundred two Korean patients with acute symptomatic SSDIs underwent
cerebral angiography or magnetic resonance angiography and echocardiography.
We divided these patients into 2 groups—patients with and without MCA
occlusive lesions. The clinical and magnetic resonance image features were
compared between these 2 groups.
Results Thirty-seven patients (36%) had an ipsilateral proximal MCA lesion,
whereas 65 patients (64%) showed no MCA abnormality on cerebral angiography
or magnetic resonance angiography. Among 65 patients without an MCA lesion,
18 had an embolic source; the remaining 37 patients had no demonstrable embolic
source. There were significant differences in the temporal profile and magnetic
resonance imaging findings between the groups. Although the type of lacunar
syndrome and the volume of infarcts did not differ between the groups, the
unstable temporal profile and magnetic resonance imaging findings of multiple
small infarcts in the symptomatic hemisphere were frequently observed in patients
with MCA lesions.
Conclusions The proximal MCA lesion was a common cause of SSDIs in Korean patients.
Depending on the existence of an MCA lesion, the clinical course and magnetic
resonance imaging feature of the patients with SSDIs were different.
INTRODUCTION
SEVERAL THEORIES explain the pathogenesis of symptomatic small, deep
infarctions. Small-vessel disease resulting from hypertension is generally
thought to be the most common cause and to have characteristic clinical features
and a good prognosis. Extracranial sources of emboli, such as cardiac problems
or the atherosclerosis of the internal carotid artery, have been found in
patients with small, deep infarctions.1-2
Atherosclerosis of the middle cerebral artery (MCA) may also occlude the origin
of deep perforators resulting in striatocapsular small, deep infarctions (SSDIs).3-5 However, the frequency
of the MCA occlusive lesions, ranging from 2%1
to 21%,6 in patients with SSDIs has rarely
been described. Previous studies have shown that atherosclerotic involvement
of the intracranial vessels occur more frequently in Asian patients than in
Westerners.3, 5 Therefore, the
frequency of the MCA occlusive lesions with SSDIs may be more prevalent in
Asian patients. However, to our knowledge, this has not yet been reported.
It is important to define the pathogenesis of MCA stenosis, because
a different treatment may be warranted. Moreover, because the high risk of
stroke has been reported if associated MCA stenosis is present,3
the detection of an MCA occlusive lesion in patients with SSDIs may achieve
major significance in clinical practice.
We, therefore, retrospectively reviewed the findings of cerebral angiography,
magnetic resonance angiography (MRA), and magnetic resonance imaging (MRI)
in patients with acute symptomatic SSDIs. The aim of this study was to compare
the clinical features and MRI findings of patients who have acute symptomatic
SSDIs with and without MCA occlusive lesions.
PATIENTS AND METHODS
From January 6, 1996, to May 25, 2001, we retrospectively studied consecutive
patients with acute symptomatic SSDIs. The inclusionary criteria were as follows:
patients who had suffered traditional lacunar syndrome and who had been observed
within 1 week after the onset of symptoms, those who underwent cerebral angiography
or MRA within 2 weeks after the onset of symptoms, and those who had MRI-confirmed
relevant focal small (<15-mm), deep infarcts within the striatocapsular
area. Of the patients who had multiple lesions or no abnormalities on MRI,
we selected only those who underwent diffusion-weighted MRI.
Of 292 patients who suffered from lacunar syndrome and had small, deep
infarcts on MRI during the study period, 102 composed the cohort. The primary
reasons for exclusion were as follows: (1) small, deep infarcts located outside
striatocapsular area (ie, the territory of the posterior circulation, superficial
pial MCA, or anterior choroidal artery) (n = 142 patients); (2) no documentation
of a relevant lesion on MRI but the patient did not undergo diffusion-weighted
MRI (n = 6 patients); (3) SSDIs associated with specific disease process4 (n = 7 patients); or (4) no undergo either cerebral
angiography or MRA within 2 weeks after the onset of symptoms (n = 35 patients).
We divided the patients into 2 groups according to angiographic findings.
The first group included patients with mural atheroma at the proximal MCA
(M1), which showed an occlusive lesion at the origin of MCA penetrating arteries
on cerebral angiography or MRA. The second group included those who had a
normal MCA on cerebral angiography or MRA.
We reviewed the medical history, general physical and neurological examination
findings, and laboratory test results. National Institutes of Health Stroke
Scale (NIHSS) score7 was checked at admission
to the hospital as well as on days 1, 3, and 7 after admission. Clinical course
was determined after a 1-week follow-up period and defined as follows: improved,
when the NIHSS score decreased more than 2 points; stable, when the score
decreased less than 2 points; worsening, when the score increased after admission;
and fluctuating, when the score episodically increased and then decreased
or vice versa. Electrocardiography was performed in all patients, and echocardiography
was performed in 77 patients, especially when the possibility of cardioembolic
sources was suggested or when no other cause of stroke was found.
Brain MRI (1.5 T) was performed in all patients and diffusion-weighted
MRI in 78 patients. The diagnosis of infarcts in the striatocapsular distribution
was made with the use of previously published templates.8
The volume of the lesion was calculated from the MRI using the methods of
Nelson et al.9 Cerebral angiography was performed
in 40 patients and MRA in the remaining 62 patients. We measured M1 stenosis
on MRA or conventional angiography by previously suggested methods.10-11 The M1 stenosis was calculated according
to the residual luminal diameter measured at the site of maximal narrowing
and the diameter of the adjacent normal vessel, from which a percentage of
stenosis was calculated. The degree of stenosis was graded as follows: lower
degree of stenosis (50%-69%) or higher degree of stenosis ( 70%). All patients
who were classified as having a higher degree of stenosis on MRA had segmental
loss of signal at the stenotic site. In the patients who underwent MRA, ultrasonography
or MRA of the carotid artery was also performed. Internal carotid artery stenosis
was calculated using the North American Symptomatic Carotid Endarterectomy
Trial study method.12  2 Test
and t test were used to compare clinical and radiological
findings between the 2 groups.
RESULTS
Among the 102 patients, 68% were men and 32% were women, and their ages
ranged from 35 to 85 years (mean age, 58 years). The angiographic and echocardiographic
findings are listed in Table 1.
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Table 1. Angiographic Classification of 102 Patients With Striatocapsular
Small, Deep Infarctions*
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Thirty-seven (36%) of the 102 patients had a symptomatic MCA lesion.
The lesions were disclosed in 20 patients by cerebral angiography and in 17
patients by MRA. Twenty-one patients had a high degree of stenosis; 16 patients
had a lower degree of stenosis.
Embolic sources from the internal carotid artery, aorta, and heart were
found in 25 patients (25%). Cardiac sources included atrial fibrillation,
congestive heart failure with aortic arch atheroma (AAA), AAA with patent
foramen ovale, AAA with atrial fibrillation, akinetic left ventricular segment,
and aortic stenosis with cardiac thrombi. The patients who had MCA more often
had embolic sources than those who had a stenotic MCA.
CLINICAL FEATURES
None had cortical dysfunction, such as aphasia or agnosia. Faciobrachiocrural
involvement was characteristic, except for the patients with dysarthria clumsy
hand syndrome or ataxic hemiparesis (Table
2). The age, sex ratio, the risk factors for stroke, and the types
of the lacunar syndrome were not different between the groups.
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Table 2. Clinical and Radiological Features in Each Group of Patients*
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However, unstable clinical courses (fluctuating or worsening) were significantly
more common in the patients with MCA lesions (14 patients [38%]) compared
with those without it (8 patients [12%]). The frequency of such an unstable
temporal profile was higher in the patients with a higher degree of M1 stenosis
(48%) than in those with a lower degree of stenosis (25%). A history of previous
transient ischemic attack (TIA) was also more frequent in patients with MCA
lesions (14 patients [38%]) than in those without them (11 patients [17%]).
In the patients without an MCA lesion, the frequency of unstable clinical
course or TIA was unrelated to the embolic sources.
MRI FINDINGS
Multiple small infarctions in the symptomatic hemispheric area were
found in 23 patients (Figure 1 and Table 2). In 12 of 78 patients who underwent
diffusion-weighted MRI, incidental small ischemic lesions were detected outside
the striatocapsular area. Ten patients had proximal embolic sources (patients
2 through 4; Figure 1, B) or a high
degree of MCA stenosis (patients 6 through 12; Figure 1, D). In the remaining 11 patients, multiple small, deep
infarctions were found within the striatocapsular area of the symptomatic
side, and 8 of them had ipsilateral MCA lesion of either degree (patients
1 through 3, Figure 1, C and patients
1 through 5, Figure 1, D). No significant
difference in the size or volume of each ischemic lesion and white matter
changes were found between the 2 groups.
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Diffusion-weighted imaging and angiographic findings in the patients
with unilateral multiple small infarcts. A, View of a normal middle cerebral
artery (MCA) and no embolic source. MRA indicates magnetic resonance angiography.
B, View of an embolic source but no MCA occlusive lesion. TFCA indicates transfemoral
conventional angiography. C, View of a lesser degree of MCA stenosis. D, View
of a higher degree of MCA stenosis.
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COMMENT
In this study, about 40% of the patients with SSDIs had stenotic lesions
of the MCA, which is a parent artery of the lenticulostriate arteries. Intracranial
stenosis has been reported to be neglected as a cause of small, deep infarction1; however, about half of the patients who had MCA stenosis
also had small, deep infarctions.13-14
Findings from our present study suggest that large-artery atherosclerosis
and small arterial abnormalities may present with symptomatic SSDIs in a significant
fraction of patients. Since intracranial atheroscleosis is more common in
Asians than in Westerners, who are known to have extracranial stenosis more
frequently,1, 3, 5, 15
it is conceivable that intracranial stenosis may play an important role in
the development of small, deep infarctions in Asians.15
Patients with stenotic MCA lesions showed clinical characteristics distinct
from those with the normal MCA. A history of TIA and temporal profile of fluctuation
or worsening of symptoms were frequent in the patients with stenotic MCA lesions.
Fisher16 reported that vascular stenosis was
associated with an unstable clinical course. Capsular lacunar syndromes with
prior ipsilateral TIA were not benign and indicated large-vessel disease of
either the MCA or the internal carotid artery.5
Our findings, in agreement with published data, suggest that patients with
small, deep infarction associated with occlusive diseases of the parent artery
may experience unstable clinical courses.
With the introduction of the diffusion-weighted imaging, silent infarctions
at different sites from the symptomatic small, deep infarction could be detected.
Multiple infarctions on the ipsilateral striatocapsular area or cortical and
subcortical areas supplied by the MCA were other distinct features of severe
MCA stenosis. Thromboembolism from the atherosclerotic plaque of the MCA might
be responsible for the frequent association of multiple infarctions in the
patients with severe MCA stenosis. Multiple small lesions on diffusion-weighted
MRI were reported to be more likely to harbor an identifiable stroke mechanism
than a single small, deep infarction.17
Several limitations of our present study deserve to be mentioned. Although
proximal embolic sources were not found in most of the patients with an MCA
lesion, a signal gap in the MRA or even a narrowing in the angiogram may represent
only a partially recanalized clot. Also, there may be a discrepancy in the
degree of stenosis between MRA and angiogram. None of our patients underwent
both MRA and conventional angiogram.
CONCLUSIONS
Striatocapsular small infarctions were frequently associated with occlusive
lesions of the MCA, which may require diagnostic and therapeutic approach
different from the small arterial disease of good prognosis. A history of
preceding TIA, fluctuating or progressive clinical courses, and ipsilateral
multiple infarctions on MRI are findings that strongly suggest occlusive lesions
of the MCA.
AUTHOR INFORMATION
Accepted for publication September 18, 2001.
Author contributions: Study concept and design (Drs Bang and Huh); acquisition of data (Drs Bang, Kim, and Park); analysis and interpretation of data (Drs Bang and Heo); drafting of the manuscript (Drs Bang, Kim, and Park); critical revision of the manuscript for
important intellectual content (Drs Heo and Huh);
statistical expertise (Dr Bang); administrative,
technical, and material support (Dr Kim, Park, and Huh); and study supervision (Drs Heo and Huh).
Corresponding author and reprints: Kyoon Huh, MD, Department of Neurology,
College of Medicine, Ajou University, Woncheon-dong San 5, Paldal-ku, Suwon,
Kyungki-do 442-749, South Korea (e-mail: khuh{at}madang.ajou.ac.kr).
From the Departments of Neurology, College of Medicine, Ajou University,
Suwon (Drs Bang and Huh); College of Medicine, Yonsei University, Seoul (Dr
Heo); and the College of Medicine, InJe University, Seoul (Drs Kim and Park),
South Korea.
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