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Aging and disease    2018, Vol. 9 Issue (6) : 1074-1083     DOI: 10.14336/AD.2018.0118
Orginal Article |
Association between Leukoaraiosis and Symptomatic Intracranial Large Artery Stenoses and Occlusions: the Chinese Intracranial Atherosclerosis (CICAS) Study
Duan Wanying1,2,3,4, Pu Yuehua1,2,3,4, Liu Haiyan1,2,3,4,5, Jing Jing1,2,3,4, Pan Yuesong1,2,3,4,6, Zou Xinying1,2,3,4, Wang Yilong1,2,3,4, Zhao Xingquan1,2,3,4, Wang Chunxue1,2,3,4, Wang Yongjun1,2,3,4, Wong Ka Sing Lawrence7, Wei Ling8,9, Liu Liping1,2,3,4,*, on behalf of the CICAS StudyGroup
1Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
2China National Clinical Research Center for Neurological Diseases, Beijing, China.
3Center of Stroke, Beijing Institute for Brain Disorders, China.
4Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease, Beijing, China.
5Department of Neurology, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
6Department of Epidemiology and Health Statistics, School of Public Health, Capital Medical University, Beijing, China.
7Department of Medicine and Therapeutics, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong Special Administrative Region, China.
8Department of Anesthesiology, Emory University School of Medicine, Atlanta, GA, USA.
9Department of Neurology, Emory University School of Medicine, Atlanta, GA, USA.
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Leukoaraiosis (LA) is frequently found in ischemic stroke patients, especially when those patients have intracranial atherosclerosis (ICAS). However, previous studies regarding an association of LA with cerebral large artery atherosclerosis showed conflicting results, and the relationship of LA with ICAS is uncertain. This study aimed to explore the association between LA and cerebral large artery atherosclerosis in Chinese patients with cerebral ischemia. Data were derived from the Chinese Intracranial Atherosclerosis (CICAS) study. Patients diagnosed with an ischemic stroke or transient ischemic attack (TIA) within 7 days of symptom onset were included. The analysis of magnetic resonance imaging (MRI) focused on severity of LA in periventricular and deep white matter; type of cerebral large artery stenosis; and the number, severity, and distribution of ICAS lesions. ICAS was defined as an occlusion or more than 50% stenosis of intracranial vessels on magnetic resonance angiography. Among 2420 patients included, distinct LA was observed in 898 (37.11%) patients, and the rate of LA increased significantly with an increased number of risk factors. Multivariate analysis revealed that LA was independently associated with ICAS (odds ratio [OR], 1.388; 95% confidence interval [CI], 1.132-1.702; P=0.0016). In the subgroup analysis of ICAS, LA was more frequently observed in multiple lesions (OR, 1.342; 95% CI, 1.060-1.699; P=0.0146), occlusive lesions (OR, 1.554; 95% CI, 1.214-1.998; P=0.0005), and lesions in the posterior circulation (OR, 1.360; 95% CI, 1.003-1.846; P=0.0481). In this nationwide prospective study, LA was associated with symptomatic ICAS, patients with multiple ICAS lesions, occlusive lesions, and atherosclerotic lesions in the posterior circulation were more likely to coexist with LA.

Keywords leukoaraiosis      intracranial arteriosclerosis      magnetic resonance imaging      ischemia     
Corresponding Authors: Liu Liping   
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These authors contributed equally to this work.

Issue Date: 30 December 2017
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Duan Wanying
Pu Yuehua
Liu Haiyan
Jing Jing
Pan Yuesong
Zou Xinying
Wang Yilong
Zhao Xingquan
Wang Chunxue
Wang Yongjun
Wong Ka Sing Lawrence
Wei Ling
Liu Liping
on behalf of the CICAS StudyGroup
Cite this article:   
Duan Wanying,Pu Yuehua,Liu Haiyan, et al. Association between Leukoaraiosis and Symptomatic Intracranial Large Artery Stenoses and Occlusions: the Chinese Intracranial Atherosclerosis (CICAS) Study[J]. Aging and disease, 2018, 9(6): 1074-1083.
URL:     OR
Without LA
With LA
p value
Age*, y61.9±11.259.0±11.167.2±9.2<0.0001
Male sex1634 (67.52)1037 (68.13)597 (66.48)0.4021
Hypertension1884 (77.85)1115 (73.26)769 (85.63)<0.0001
Diabetes mellitus858 (35.45)522 (34.30)336 (37.42)0.1218
Hyperlipidemia1841 (76.07)1179 (77.46)662 (73.72)0.0378
Heart disease228 (7.96)145 (7.38)83 (9.24)0.0906
Peripheral vascular disease17 (0.70)14 (0.92)3 (0.33)0.0779
Family history of stroke250 (10.33)166 (10.91)84 (9.35)0.2225
History of cerebral ischemia1745 (72.11)957 (62.88)788 (87.75)<0.0001
History of hemorrhage stroke43 (1.78)11 (0.72)32 (3.56)<0.0001
Current smoker854 (35.29)601 (39.49)253 (28.17)<0.0001
Heavy drinker113 (4.67)88 (5.78)25 (2.78)0.0005
Multiple infarctions260 (14.12)171 (15.00)89 (12.68)0.1620
Pattern of infarct0.0036
 No infarct552 (23.07)368 (24.42)184 (20.77)
 Supratentorial1382 (57.76)855 (56.73)527 (59.48)
 Infratentorial423 (17.68)264 (17.52)159 (17.95)
 Supratentorial and infratentorial36 (1.50)20 (1.33)16 (1.81)
Lacune980 (40.50)410 (26.94)570 (63.47)<0.0001
Cerebral microbleeds192 (7.93)64 (4.20)128 (14.25)<0.0001
Complete circle of Willis120 (4.96)89 (5.85)31 (3.45)0.0071
Table 1  Baseline Characteristics of Participants.
OR (95% CI)p Value
Age1.075 (1.064-1.086)<0.0001
Hypertension1.316 (1.018-1.702)0.0361
Hyperlipidemia0.877 (0.700-1.100)0.2570
History of cerebral ischemic2.224 (1.704-2.902)<0.0001
History of hemorrhage stroke5.072 (2.333-11.028)<0.0001
Current smoker0.862 (0.690-1.077)0.1918
Heavy drinker0.633 (0.371-1.082)0.0947
Infratentorial infarct pattern1.505 (1.160-1.953)0.0021
Lacune3.154 (2.555-3.895)<0.0001
Cerebral microbleeds2.537 (1.776-3.625)<0.0001
Complete circle of Willis0.867 (0.538-1.396)0.5567
Table 2  Independent Association Between Leukoaraiosis and Baseline Characteristics.
Without LA
With LA
p value
ICAS1155 (47.73)675 (44.35)480 (53.45)<0.0001
Distribution of stenosis0.0002
 None1146 (47.36)765 (50.26)381 (42.43)
 Intracranial only930 (38.43)549 (36.07)381 (42.43)
 Extracranial only119 (4.92)82 (5.39)37 (4.12)
 Intracranial and extracranial225 (9.30)126 (8.28)99 (11.02)
Multiple ICAS*517 (21.36)283 (18.59)234 (26.06)<0.0001
Severity of ICAS†0.0007
 None or <50%1265 (52.27)847 (55.65)418 (46.55)
 50% to 69%290 (11.98)163 (10.71)127 (14.14)
 70% to 99%218 (9.01)129 (8.48)89 (9.91)
 100%647 (26.74)383 (25.16)264 (29.40)
Distribution of ICAS‡<0.0001
 None1265 (52.27)847 (55.65)418 (46.55)
 Anterior569 (23.51)376 (24.70)193 (21.49)
 Posterior289 (11.94)156 (10.25)133 (14.81)
 Anterior and posterior297 (12.27)143 (9.40)154 (17.15)
Table 3  ICAS Characteristics of Patients with and without LA.
Figure 1.  Percentage of patients with leukoaraiosis according to the distribution of stenosis and number of vascular risk factors. The number above each block indicates the percentage of patients with leukoaraiosis. MRA, magnetic resonance angiography.
OR (95% CI)
p valueAdjusteda
OR (95% CI)
p value
ICAS1.441 (1.221-1.700)<0.00011.388 (1.132-1.702)0.0016
Distribution of stenosis
 Intracranial only1.393 (1.165-1.667)0.00031.320 (1.060-1.644)0.0132
 Extracranial only0.906 (0.603-1.361)0.6347--
 Intracranial and extracranial1.578 (1.180-2.109)0.00211.405 (0.988-1.998)0.0581
Multiple ICAS*1.543 (1.267-1.879)<0.00011.342 (1.060-1.699)0.0146
Severity of ICAS
 None or <50%1
 50% to 69%1.579 (1.217-2.047)0.00061.308 (0.959-1.783)0.0898
 70% to 99%1.398 (1.041-1.877)0.02571.136 (0.805-1.603)0.4690
 100%1.397 (1.148-1.699)0.00081.554 (1.214-1.998)0.0005
Distribution of ICAS
 Anterior1.040 (0.844-1.282)0.7129--
 Posterior1.728 (1.333-2.239)<0.00011.360 (1.003-1.846)0.0481
 Anterior and posterior2.182 (1.689-2.819)<0.00011.769 (1.304-2.400)0.0002
Table 4  Association Between Leukoaraiosis and ICAS.
[1] Pantoni L (2002). Pathophysiology of age-related cerebral white matter changes. Cerebrovasc Dis, 13 Suppl 2: 7–10.
[2] Debette S, Markus HS (2010). The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis. BMJ, 341: c3666.
[3] Gupta A, Nair S, Schweitzer AD, Kishore S, Johnson CE, Comunale JP, et al. (2012). Neuroimaging of cerebrovascular disease in the aging brain. Aging Dis, 3: 414–425.
[4] Vermeer SE, Prins ND, den Heijer T, Hofman A, Koudstaal PJ, Breteler MM (2003). Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med, 348: 1215–1222.
[5] Fu JH, Lu CZ, Hong Z, Dong Q, Luo Y, Wong KS (2005). Extent of white matter lesions is related to acute subcortical infarcts and predicts further stroke risk in patients with first ever ischaemic stroke. J Neurol Neurosurg Psychiatry, 76: 793–796.
[6] Kim GM, Park KY, Avery R, Helenius J, Rost N, Rosand J, et al. (2014). Extensive leukoaraiosis is associated with high early risk of recurrence after ischemic stroke. Stroke, 45: 479–485.
[7] Wong TY, Klein R, Sharrett AR, Couper DJ, Klein BE, Liao DP, et al. (2002). Cerebral white matter lesions, retinopathy, and incident clinical stroke. JAMA, 288: 67–74.
[8] Hijdra A, Verbeeten B, Jr., Verhulst JA (1990). Relation of leukoaraiosis to lesion type in stroke patients. Stroke, 21: 890–894.
[9] Rost NS, Rahman RM, Biffi A, Smith EE, Kanakis A, Fitzpatrick K, et al. (2010). White matter hyperintensity volume is increased in small vessel stroke subtypes. Neurology, 75: 1670–1677.
[10] Bots ML, van Swieten JC, Breteler MM, de Jong PT, van Gijn J, Hofman A, et al. (1993). Cerebral white matter lesions and atherosclerosis in the Rotterdam Study. Lancet, 341: 1232–1237.
[11] Park JH, Kwon HM, Lee J, Kim DS, Ovbiagele B (2015). Association of intracranial atherosclerotic stenosis with severity of white matter hyperintensities. Eur J Neurol, 22: 44–52, e42–43.
[12] Nam KW, Kwon HM, Jeong HY, Park JH, Kim SH, Jeong SM, et al. (2017). Cerebral white matter hyperintensity is associated with intracranial atherosclerosis in a healthy population. Atherosclerosis, 265: 179–183.
[13] Wang Y, Zhao X, Liu L, Soo YO, Pu Y, Pan Y, et al. (2014). Prevalence and outcomes of symptomatic intracranial large artery stenoses and occlusions in China: the Chinese Intracranial Atherosclerosis (CICAS) Study. Stroke, 45: 663–669.
[14] Zhang C, Wang Y, Zhao X, Wang D, Liu L, Wang C, et al. (2014). Distal single subcortical infarction had a better clinical outcome compared with proximal single subcortical infarction. Strok, 45: 2613–2619.
[15] Wardlaw JM, Smith EE, Biessels GJ, Cordonnier C, Fazekas F, Frayne R, et al. (2013). Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol, 12: 822–838.
[16] Pantoni L, Simoni M, Pracucci G, Schmidt R, Barkhof F, Inzitari D (2002). Visual rating scales for age-related white matter changes (leukoaraiosis): can the heterogeneity be reduced? Stroke, 33: 2827–2833.
[17] Lee SJ, Kim JS, Lee KS, An JY, Kim W, Kim YI, et al. (2008). The leukoaraiosis is more prevalent in the large artery atherosclerosis stroke subtype among Korean patients with ischemic stroke. BMC Neurol, 8: 31–36.
[18] Zhu YC, Dufouil C, Tzourio C, Chabriat H (2011). Silent brain infarcts: a review of MRI diagnostic criteria. Stroke, 42: 1140–1145.
[19] Werring DJ, Coward LJ, Losseff NA, Jager HR, Brown MM (2005). Cerebral microbleeds are common in ischemic stroke but rare in TIA. Neurology, 65: 1914–1918.
[20] Samuels OB, Joseph GJ, Lynn MJ, Smith HA, Chimowitz MI (2000). A standardized method for measuring intracranial arterial stenosis. AJNR Am J Neuroradiol, 21: 643–646.
[21] Grant EG, Benson CB, Moneta GL, Alexandrov AV, Baker JD, Bluth EI, et al. (2003). Carotid artery stenosis: grayscale and Doppler ultrasound diagnosis--Society of Radiologists in Ultrasound consensus conference. Ultrasound Q, 19: 190–198.
[22] Pu Y, Liu L, Wang Y, Zou X, Pan Y, Soo Y, et al. (2013) Geographic and sex difference in the distribution of intracranial atherosclerosis in China. Stroke, 44: 2109–2114.
[23] van Raamt AF, Mali WP, van Laar PJ, van der Graaf Y (2006). The fetal variant of the circle of Willis and its influence on the cerebral collateral circulation. Cerebrovasc Dis, 22: 217–224.
[24] Caplan L, Wityk R, Pazdera L, Chang HM, Pessin M, Dewitt L (2005). New England Medical Center Posterior Circulation Stroke Registry II. Vascular Lesions. J Clin Neurol, 1: 31–49.
[25] Wang W, Jiang B, Sun H, Ru X, Sun D, Wang L, et al. (2017). Prevalence, Incidence, and Mortality of Stroke in China: Results from a Nationwide Population-Based Survey of 480 687 Adults. Circulation, 135: 759–771.
[26] Wang W, Wang D, Liu H, Sun H, Jiang B, Ru X, et al. (2017). Trend of declining stroke mortality in China: reasons and analysis. Stroke Vasc Neurol, 2(3): 132–139.
[27] Wong KS, Li H, Chan YL, Ahuja A, Lam WW, Wong A, et al. (2000). Use of transcranial Doppler ultrasound to predict outcome in patients with intracranial large-artery occlusive disease. Stroke, 31: 2641–2647.
[28] De Silva DA, Woon FP, Lee MP, Chen CP, Chang HM, Wong MC (2007). South Asian patients with ischemic stroke: intracranial large arteries are the predominant site of disease. Stroke, 38: 2592–2594.
[29] Lee SJ, Kim JS, Lee KS, An JY, Kim W, Kim YI, et al. (2008). The leukoaraiosis is more prevalent in the large artery atherosclerosis stroke subtype among Korean patients with ischemic stroke. BMC Neurol, 8: 31–36.
[30] Bots ML, van Swieten JC, Breteler MM, de Jong PT, van Gijn J, Hofman A, et al. (1993). Cerebral white matter lesions and atherosclerosis in the Rotterdam Study. Lancet, 341: 1232–1237.
[31] de Leeuw FE, de Groot JC, Bots ML, Witteman JC, Oudkerk M, Hofman A, et al. (2000). Carotid atherosclerosis and cerebral white matter lesions in a population based magnetic resonance imaging study. J Neurol, 247: 291–296.
[32] Altaf N, Daniels L, Morgan PS, Lowe J, Gladman J, MacSweeney ST, et al. (2006). Cerebral white matter hyperintense lesions are associated with unstable carotid plaques. Eur J Vasc Endovasc Surg, 31: 8–13.
[33] Bogousslavsky J, Regli F, Uske A (1987). Leukoencephalopathy in patients with ischemic stroke. Stroke, 18: 896–899.
[34] Wiszniewska M, Devuyst G, Bogousslavsky J, Ghika J, van Melle G (2000). What is the significance of leukoaraiosis in patients with acute ischemic stroke? Arch Neurol, 57: 967–973.
[35] Pu Y, Liu L, Zou X, Chen P, Wang Y, Zhou Y, et al. (2013). Relationship between leukoaraiosis and cerebral large artery stenosis. Neurol Res, 31: 376–380.
[36] Pantoni L, Garcia JH (1997). Pathogenesis of leukoaraiosis: a review. Stroke, 28: 652–659.
[37] Li H, Xu G, Xiong Y, Zhu W, Yin Q, Fan X, et al. (2014). Relationship between cerebral atherosclerosis and leukoaraiosis in aged patients: results from DSA. J Neuroimaging, 24; 338–342.
[38] Marstrand JR, Garde E, Rostrup E, Ring P, Rosenbaum S, Mortensen EL, et al. (2002). Cerebral perfusion and cerebrovascular reactivity are reduced in white matter hyperintensities. Stroke, 33: 972–976.
[39] Fisher CM, Gore I, Okabe N, White PD (1965). Calcification of the carotid siphon. Circulation, 32: 538–548.
[40] Baker AB, Iannone A (1959). Cerebrovascular disease. I. The large arteries of the circle of Willis. Neurology, 9: 321–332.
[41] Moossy J (1966). Morphology, sites and epidemiology of cerebral atherosclerosis. Res Publ Assoc Res Nerv Ment Dis, 41: 1–22.
[42] Amarenco P, Hauw JJ, Gautier JC (1990). Arterial pathology in cerebellar infarction. Stroke, 21: 1299–1305.
[43] Fisher CM, Karnes WE, Kubik CS (1961). Lateral medullary infarction-the pattern of vascular occlusion. J Neuropathol Exp Neurol, 20: 323–379.
[44] Hauw JJ, Der Agopian P, Trelles L, Escourolle R (1976). Bulbar infarcts. Systematic study of lesion topography in 49 cases. J Neurol Sci, 28: 83–102.
[45] Klein IF, Lavallee PC, Mazighi M, Schouman-Claeys E, Labreuche J, Amarenco P (2010). Basilar artery atherosclerotic plaques in paramedian and lacunar pontine infarctions: a high-resolution MRI study. Stroke, 41: 1405–1409.
[46] Caplan L, Wityk R, Pazdera L, Chang HM, Pessin M, Dewitt L (2005). New England Medical Center Posterior Circulation Stroke Registry II. Vascular Lesions. J Clin Neurol, 1: 31–49.
[47] Bogousslavsky J, Regli F, Maeder P, Meuli R, Nader J (1993). The etiology of posterior circulation infarcts: a prospective study using magnetic resonance imaging and magnetic resonance angiography. Neurology, 43: 1528–1533.
[48] von Sarnowski B, Schminke U, Grittner U, Tanislav C, Bottcher T, Hennerici MG, et al. (2017). Posterior versus Anterior Circulation Stroke in Young Adults: A Comparative Study of Stroke Aetiologies and Risk Factors in Stroke among Young Fabry Patients (sifap1). Cerebrovasc Dis, 43: 152–160.
[49] Leys D, Englund E, Del Ser T, Inzitari D, Fazekas F, Bornstein N, et al. (1999). White matter changes in stroke patients. Relationship with stroke subtype and outcome. Eur Neurol, 42: 67–75.
[50] Chutinet A, Biffi A, Kanakis A, Fitzpatrick KM, Furie KL, Rost NS (2012). Severity of leukoaraiosis in large vessel atherosclerotic disease. AJNR Am J Neuroradiol, 33: 1591–1595.
[51] Valdés Hernández MdC, Morris Z, Dickie DA, Royle NA, Muñoz Maniega S, Aribisala BS, et al. (2013). Close correlation between quantitative and qualitative assessments of white matter lesions. Neuroepidemiology, 40: 13–22.
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