(Stroke. 1999;30:378-382.)
© 1999 American Heart Association, Inc.
Original Contributions |
From the Neurology Service (T.U., M.T.), Hyogo Brain and Heart Center at Himeji, and Department of Clinical Neurosciences, Hyogo Institute for Aging Brain and Cognitive Disorders (E.M.), Himeji, Japan.
Correspondence to Toshiyuki Uehara, MD, Neurology Service, Hyogo Brain and Heart Center at Himeji, 520 Saisho-ko, Himeji, 670-0981, Japan. E-mail tuehara{at}hbhc.hiabcd.go.jp
| Abstract |
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MethodsSubjects of this study were 219 adults without a history of stroke or transient ischemic attack and without any abnormality on a neurological examination who consecutively visited the neurology service in our hospital between January 1994 and November 1997 requesting medical evaluation for possible cerebrovascular diseases. Subjects included 141 men and 78 women ranging in age from 33 to 83 years (mean±SD, 63.2±9.5 years). We performed brain MRIs and cervical/cranial MR angiographies on all subjects. In this study, SCI was defined as a focal lesion >5 mm in diameter that was prolonged on both T2-weighted and proton density images.
ResultsSCIs in the WM and/or BG were detected in 88 (40.2%) of the 219 subjects. No SCI >15 mm was observed in this series. Fifty of the subjects had SCIs only in the WM, 32 subjects had SCIs in both the WM and BG, and 6 subjects had SCIs only in the BG. Thus, 82 (93.2%) of 88 subjects with SCIs had lesions in the WM. Most subjects with SCIs in the BG also had SCIs in the WM. Multiple logistic regression analyses revealed that age, female sex, and hypertension were significant and independent predictors of SCIs in the WM, and that age, a history of ischemic heart disease, and carotid artery stenosis were significant and independent predictors of SCIs in the BG.
ConclusionsThe present study indicated that the relevant risk factors for SCIs in the WM and those for SCI in the BG were different. Our results suggest that SCIs are prone to first appear in the WM in association with aging and hypertension, and the additional appearance of SCIs in the BG predicts a progression of generalized atherosclerosis that is manifested in the carotid and coronary arteries.
Key Words: infarcts, silent magnetic resonance angiography magnetic resonance imaging risk factors
| Introduction |
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| Subjects and Methods |
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We performed brain MRI and MR angiography (MRA) on all subjects. All
examinations were performed with a 1.0-T MR system (Magnetom Impact,
Siemens). T1-weighted images (repetition time, 500 ms; echo time, 15
ms), T2-weighted images (repetition time, 2000 ms; echo time, 80 ms),
and proton density images (repetition time, 2000 ms; echo time, 20 ms)
were obtained in the transverse plane with 8-mm-thick sections. An SCI
was defined as a focal lesion >5 mm in diameter that was
prolonged on both T2-weighted and proton density images.
Periventricular hyperintense lesions and subcortical patchy
or confluent hyperintense lesions were not included. When distinction
between such lesions and infarcts was ambiguous, we used T1-weighted
images, in which infarcts are primarily presented with
hypodensity. We recorded the presence of
1 SCI in the territory
of the carotid artery system in each subject. The location was coded
separately as WM or BG.
MRA acquisition and reconstruction are described
elsewhere.9 10 11 The extracranial portion of the internal
carotid artery (ICA) was evaluated with cervical MRA. To measure the
percent stenosis of the extracranial portion of the ICA, we
compared the diameter of maximal stenosis with that of the
normal-appearing proximal ICA beyond the carotid bulb.12
The intracranial arteries were evaluated with intracranial MRA for the
intracranial portion of the ICA and the horizontal portion of the
middle cerebral artery (MCA). We rated occlusive lesions for each
arterial portion by giving them 1 of 5 grades depending on
the narrowness of the arteries, ie, normal, mild, moderate, severe, and
occluded according to an established scoring scheme.9 10
In this scoring scheme, <25% reduction of an arterial
diameter was graded as normal, 25% to 49% reduction was graded as
mild stenosis, 50% to 74% reduction was graded as moderate
stenosis, 75% to 99% reduction was graded as severe
stenosis, and no opening was graded as occlusion. Two
investigators (T.U., M.T.), under blinded conditions for all clinical
information, independently reviewed the MRIs and MRAs. When there was
disagreement, the final decision was made through a consensus meeting
with a third investigator (E.M.). Interrater reliability and accuracy
are good for evaluating stenoses of >25% narrowing in the
cervical carotid artery and specific segments of the intracranial
arteries. For the carotid bifurcation, the reliability (
=0.89) and
accuracy are comparable to those of conventional
angiography.10 For the intracranial arteries,
substantially high interrater reliability (
=0.85) and specificity
(>85%) have been achieved as well as a sensitivity of
100%.9
Hypertension, diabetes mellitus, hyperlipidemia, smoking habit, and ischemic heart disease (IHD) were evaluated as risk factors. Hypertension was judged as present when either systolic pressure of >160 mm Hg or diastolic pressure of >95 mm Hg was demonstrated on repeated examinations or when there was a history of treatment for hypertension. Diabetes mellitus was judged as present when a fasting blood glucose level was >140 mg/dL or when there was a history of treatment for diabetes mellitus. Hyperlipidemia was judged as present when laboratory examination of the serum at presentation showed a total cholesterol level of >220 mg/dL, a triglyceride level of >150 mg/dL, an HDL cholesterol level of <40 mg/dL, or when there was a history of treatment. IHD was judged as present when there was a history of myocardial infarction or angina pectoris.
Effects of the predictive variables on SCIs were preliminarily analyzed with Fisher exact probability test or Student's t test. Multiple logistic regression analysis was used to estimate independent effects of the predictive variables on SCIs. The analysis was repeated for each of the SCIs in the WM and BG, with each abnormality as a dependent variable and with patients' background characteristics, including possible risk factors and cerebral artery occlusive lesions, as independent variables. All statistical analyses were performed with SAS Release 6.10 software. The level of significance was set at P<0.05 for all statistical analyses.
| Results |
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Of the 219 subjects, 102 (46.6%) were hypertensive, 37 (16.9%) were diabetic, 76 (34.7%) were hyperlipidemic, 88 (40.2%) had a smoking habit, and 63 (28.8%) had IHD.
The MRA examinations indicated that 24 subjects (11.0%) had stenoses in the cervical carotid artery. Of these 24 subjects, 15 had a mild stenosis, 6 had a moderate stenosis, 2 had a severe stenosis, and 1 had an occlusion. Stenoses in the intracranial artery were found in 30 subjects (13.7%). Of these 30 subjects, 20 had a mild stenosis, 4 had a moderate stenosis, 5 had a severe stenosis, and 1 had an occlusion. Seven subjects had lesions in both the cervical carotid and intracranial arteries. Thus, the MRAs showed evidence of cerebral arterial stenoses in 46 subjects (21.0%).
The patients' characteristics, including possible risk factors and
cerebral artery occlusive lesions, are summarized for SCIs in the WM in
Table 1
and for SCIs in the BG in Table 2
. Patients with SCIs in the WM were
significantly older and had significantly higher prevalence of female
sex, hypertension, diabetes mellitus, carotid artery stenosis,
and intracranial artery stenosis than those without SCI in the
WM. Compared with patients without SCIs in the BG, those with SCIs in
the BG were significantly older and had significantly higher prevalence
of hyperlipidemia, IHD, carotid artery
stenosis, and intracranial artery stenosis. Multiple
logistic regression analyses revealed that age, female sex, and
hypertension were significant and independent predictors of SCIs in the
WM (Table 3
) and that age, IHD, and
carotid artery stenosis were significant and independent
predictors of SCIs in the BG (Table 4
).
To clarify whether the relationship between SCIs in the BG and carotid
artery stenosis contributes to the direct effects from carotid
artery stenosis, prevalence of SCIs in the BG on the side of
the carotid artery lesion and prevalence on the nonlesioned side were
compared among 24 subjects with carotid artery lesions. The prevalence
of SCIs in the BG on the side of the carotid artery lesion (13/33,
39.4%) was not significantly different from that on the side without
the carotid lesion (5/15, 33.3%) (P=0.472, Fisher exact
test).
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| Discussion |
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5 mm in diameter14 and proton densityweighted MR
images, which reportedly differentiate lacunar infarcts from dilated
perivascular spaces.15 The additional confirmation of
hypodensity on T1-weighted images was applied to distinguish infarcts
from diffuse WM disease. The MRA imaging technique and the
stenosis rating scheme used in the present study have also
been validated in comparative studies with conventional
angiography.9 10
The prevalence of SCIs in the former CT or MRI studies of first-ever
stroke patients varied from 10% to 38%.1 2 16 17 18
According to large population-based studies using MRI, the prevalence
of SCIs is 11% to 28%.19 20 21 In the present
hospital-based study, the frequency of SCIs was 40.2%. It should be
noted that this frequency refers to this particular selected population
rather than a true prevalence, since it is impossible to exclude
referral or selection bias in this type of hospital-based study. The
subjects studied were considered at high risk because they were
specifically concerned about stroke for various reasons, including
positive family history and vascular risk factors. The prevalence of
SCIs would be subject to the sample constitution, eg, age, sex, race,
ethnicity, and involved risk factors. In addition, the results would be
affected by the sensitivity and specificity of the examination and the
diagnostic criteria of SCIs used in each study. The
frequency of SCIs in our study was comparable to those reported in
MRI-based studies used in Japan. Hougaku et al4 reported a
frequency of 42% in 117 patients who had
1 stroke risk factor, and
Shimada et al22 reported a frequency of 47% in 73 elderly
patients.
Multiple logistic regression analyses showed that age, female sex, and hypertension were significant and independent predictors of SCIs in the WM and that age, IHD, and carotid artery stenosis were significant and independent predictors of SCIs in the BG. These findings support the assumption that the risk factors for SCIs in the WM and BG are different. Although univariate analyses demonstrated that diabetes mellitus, carotid artery stenosis, and intracranial artery stenosis were associated with SCIs in the WM and that hyperlipidemia and intracranial artery stenosis were associated with SCIs in the BG, these associations were not found in multiple logistic regression analyses. These associations noted in univariate analyses were likely to be discounted by interaction among factors, especially by correlations with age. Although it has been reported that smoking habit is associated with SCIs in large population-based studies,19 21 this finding was not replicated in our study. This lack of association may be attributable to the relatively small sample size of our study.
The majority of previous studies1 2 3 6 7 21 demonstrated that age and hypertension strongly and independently correlated with SCIs. As in previous studies, the present study demonstrated that age was a common risk factor for SCIs in both the WM and BG. However, in our study hypertension was a significant factor for SCIs in the WM but not in the BG. These results, together with the fact that most of cases with SCIs in the BG also had SCIs in the WM, suggest that SCIs initially appear in the WM in association with aging and hypertension and subsequently appear in the BG in association with development of atherosclerosis because hypertension accelerates the pathological process in the medullary arteries supplying the WM.8
We found a significant correlation between SCIs in the WM and female sex. In a large population-based study, a correlation between SCIs and female sex has been demonstrated.21 However, male sex has been noted as a risk factor for SCIs in some studies.1 2 16 Although the association with female sex was restricted to SCIs in the WM, the reason for the discrepancy among studies is not clear. This finding should be confirmed in further studies.
Carotid artery stenosis was a significant and independent predictor of SCIs in the BG. This finding was consistent with the findings of previous reports.4 21 23 In studies of symptomatic lacunar infarction, it has been pointed out that ipsilateral carotid stenotic lesions are potential embolic sources associated with lacunar infarction in the territory of deep perforating arteries.24 25 Ghika et al26 reported that 28 of 100 patients with symptomatic lacunar infarction in the territory of the deep perforators of the carotid system had ipsilateral carotid artery stenosis. Stenotic lesions of the ICA may also play a role in the pathogenesis of lacunes through hemodynamic effects. In an animal model study, diffuse cerebral ischemia from carotid occlusion caused infarction only in the striatum, and a possible toxic effect of dopamine release in the ischemic zone has been assumed to be related to the damage.27 The similar mechanism might be involved in human diffuse cerebral ischemia. However, in the present study SCIs in the BG were just as frequent on the contralateral side of the arterial lesions as they were on the ipsilateral side of the carotid lesions, challenging the assumption that carotid artery lesions caused these SCIs. Thus, an alternative explanation is needed. Similar to our findings, the results of Brott et al28 showed that SCIs in the setting of asymptomatic carotid stenosis were not uncommon but were evenly distributed ipsilaterally and contralaterally to the stenotic artery. Sise et al,29 analyzing the incidence of preoperative SCI in patients who underwent carotid endarterectomy, noted that SCIs were commonly found in these patients but were found on the contralateral side of the target carotid artery in more than half of the cases. They suggested that carotid plaque formation and small-vessel thrombotic events were most likely parallel phenomena related to the risk factors. Longstreth et al,21 analyzing restricted subjects with lacunes affecting only 1 side of the brain in a population-based study, reported that the correlations of stenoses were not consistently stronger for ipsilateral than for contralateral lacunes. Together with these observations, our results indicated that the appearance of SCIs in the BG was more likely to be paralleled by a background atherosclerosis than by direct effects from carotid artery stenosis.
The association between IHD and SCIs has been pointed out in a few studies.7 16 30 Our in vivo results replicated the findings of the autopsy study of Tuszynski et al,31 in which myocardial infarcts were found in 52% of patients with lacunar infarcts that were most commonly located in the BG. The appearance of SCIs in the BG likely reflects an advanced stage of systemic atherosclerosis, which is manifested in the coronary artery as well as the carotid artery.
In conclusion, the present study indicated that the relevant risk factors for SCIs in the WM and the BG were different; age, hypertension, and female sex were the risk factors for SCIs in the WM, and age, a history of IHD, and carotid stenosis were the risk factors for SCIs in the BG. Our results suggest that the SCIs are prone to first appear in the WM in association with aging and hypertension, and the appearance of SCIs in the BG predicts the progression of generalized atherosclerosis.
| Acknowledgments |
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Received August 28, 1998; revision received November 2, 1998; accepted November 2, 1998.
| References |
|---|
|
|
|---|
2.
Davis PH, Clarke WR, Bendixen BH, Adams HP Jr,
Woolson RF, Culebras A. Silent cerebral infarction in patients enrolled
in the TOAST study. Neurology. 1996;46:942948.
3. Boon A, Lodder J, Heuts-van Raak L, Kessels F. Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke: relationship with index-stroke subtype, vascular risk factors, and mortality. Stroke. 1994;25:23842390.[Abstract]
4. Hougaku H, Matsumoto M, Handa N, Maeda H, Itoh T, Tsukamoto Y, Kamada T. Asymptomatic carotid lesions and silent cerebral infarction. Stroke. 1994;25:566570.[Abstract]
5.
Herderschee D, Hijdra A, Algra A, Koudstaal PJ,
Kappelle LJ, van Gijn J. Silent stroke in patients with transient
ischemic attack or minor ischemic stroke.
Stroke. 1992;23:12201224.
6.
Kobayashi S, Okada K, Koide H, Bokura H, Yamaguchi S.
Subcortical silent brain infarction as a risk factor for clinical
stroke. Stroke. 1997;28:19321939.
7. Nishino M, Sueyoshi K, Yasuno M, Yamada Y, Abe H, Hori M, Kamada T. Risk factors for carotid atherosclerosis and silent cerebral infarction in patients with coronary heart disease. Angiology. 1993;44:432440.
8.
Furuta A, Ishii N, Nishihara Y, Horie A. Medullary
arteries in aging and dementia. Stroke. 1991;22:442446.
9. Uehara T, Mori E, Tabuchi M, Ohsumi Y, Yamadori A. Detection of occlusive lesion in intracranial arteries by three-dimensional time-of-flight magnetic resonance angiography. Cerebrovasc Dis. 1994;4:365370.
10. Uehara T, Tabuchi M, Ohsumi Y, Yoneda Y, Mori E. Usefulness of three-dimensional time-of-flight MR angiography for evaluation of carotid artery bifurcation stenosis. Cerebrovasc Dis. 1995;5:199203.
11.
Uehara T, Tabuchi M, Hayashi T, Kurogane H, Yamadori A.
Asymptomatic occlusive lesions of carotid and intracranial
arteries in Japanese patients with ischemic heart disease:
evaluation by brain magnetic resonance angiography. Stroke. 1996;27:393397.
12.
North American Symptomatic Carotid
Endarterectomy Trial (NASCET) Steering Committee.
North American Symptomatic Carotid
Endarterectomy Trial: methods, patient
characteristics, and progress. Stroke. 1991;22:711720.
13.
Awad IA, Johnson PC, Spetzler RF, Hodak JA. Incidental
subcortical lesions identified on magnetic resonance imaging in the
elderly, II: postmortem pathological correlations. Stroke. 1986;17:10901097.
14. Heier LA, Bauer CJ, Schwartz L, Zimmerman RD, Morgello S, Deck MDF. Large Virchow-Robin spaces: MR-clinical correlation. AJNR Am J Neuroradiol. 1989;10:929936.[Abstract]
15. Braffman BH, Zimmerman RA, Trojanowski JQ, Gonatas NK, Hickey WF, Schlaepfer WW. Brain MR: pathologic correlation with gross and histopathology, I: lacunar infarction and Virchow-Robin spaces. AJNR Am J Neuroradiol. 1988;9:621628.
16.
Ricci S, Celani MG, La Rosa F, Righetti E, Duca E,
Caputo N. Silent brain infarctions in patients with first-ever stroke:
a community-based study in Umbria, Italy. Stroke. 1993;24:647651.
17.
Chodosh EH, Foulkes MA, Kase CS, Wolf PA, Mohr JP, Hier
DB, Price TR, Furtado JG. Silent stroke in the NINCDS Stroke Data Bank.
Neurology. 1988;38:16741679.
18.
Kase CS, Wolf PA, Chodosh EH, Zacker HB,
Kelly-Hayes M, Kannel WB, D'Agostino RB, Scampini L. Prevalence of
silent stroke in patients presenting with initial stroke: the
Framingham Study. Stroke. 1989;20:850852.
19.
Howard G, Wagenknecht LE, Cai J, Cooper L, Kraut MA,
Toole JF. Cigarette smoking and other risk factors for silent cerebral
infarction in the general population. Stroke. 1998;29:913917.
20.
Price TR, ManolioTA, Kronmal RA, Kittner SJ, Yue
NC, Robbins J, Anton-Culver H, O'Leary DH. Silent brain infarction on
magnetic resonance imaging and neurological abnormalities in
community-dwelling older adults: the Cardiovascular
Health Study. Stroke. 1997;28:11581164.
21.
Longstreth, WT Jr, Bernick C, Manolio TA, Bryan N,
Jungreis CA, Price TR. Lacunar infarcts defined by magnetic resonance
imaging of 3660 elderly people: the Cardiovascular
Health Study. Arch Neurol. 1998;55:12171225.
22.
Shimada K, Kawamoto A, Matsubayashi K, Ozawa T. Silent
cerebrovascular disease in the elderly: correlation with ambulatory
pressure. Hypertension. 1990;16:692699.
23.
Norris JW, Zhu CZ. Silent stroke and carotid
stenosis. Stroke. 1992;23:483485.
24.
Pullicino P, Nelson RF, Kendall BE, Marshall J.
Small deep infarcts diagnosed on computed tomography.
Neurology. 1980;30:10901096.
25.
Horowitz DR, Tuhrim S, Weinberger JM, Rudolph SH.
Mechanisms in lacunar infarction. Stroke. 1992;23:325327.
26.
Ghika J, Bogousslavsky J, Regli F. Infarcts in the
territory of the deep perforators from the carotid system.
Neurology. 1989;39:507512.
27. Weinberger J, Thompson L, Samii M. The significance of basal ganglia infarction. J Stroke Cerebrovasc Dis. 1995;5:611.
28. Brott T, Tomsick T, Feinberg W, Johnson C, Biller J, Broderick J, Kelly M, Frey J, Schwartz S, Blum C, Nelson JJ, Chambless L, Toole J. Baseline silent cerebral infarction in the asymptomatic carotid atherosclerosis study. Stroke. 1994;25:11221129.[Abstract]
29.
Sise MJ, Sedwitz MM, Rowley WR, Shackford SR.
Prospective analysis of carotid
endarterectomy and silent cerebral infarction in 97
patients. Stroke. 1989;20:329332.
30.
Tanaka H, Sueyoshi K, Nishino M, Ishida M, Fukunaga R,
Abe H. Silent brain infarction and coronary artery disease in
Japanese patients. Arch Neurol. 1993;50:706709.
31.
Tuszynski MH, Petito CK, Levy DE. Risk factors and
clinical manifestations of pathologically verified lacunar infarctions.
Stroke. 1989;20:990999.
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