J. Biomedical Science and Engineering, 2010, 3, 443-447
doi:10.4236/jbise.2010.35061 Published Online May 2010 (http://www.SciRP.org/journal/jbise/
Published Online May 2010 in SciRes. http://www.scirp.org/journal/jbise
Silent brain infarctions and leuko-araiosis in Chinese patients
with first-ever acute lacunar strokes
Peterus Thajeb1,2,3,4*, Wen-Yuan Lee2, Chung-Hung Shih5, Teguh Thajeb6, James Davis3, Rosanne
Harrigan3, Linda Chang3
1Center for Stroke Care and Prevention, Cathay General Hospital Sijhih, Sijhih, Taiwan, China;
2Section of Neurosurgery and Neurology, China Medical University Hospital, Taipei, Taiwan, China;
3Biomedical Science, Graduate Division, John A Burns School of Medicine, University of Hawaii at Manoa, Hawaii, USA;
4Faculty of Medicine, National Yang-Ming University, Taipei, Taiwan, China;
5Institute of Respiratory Therapy, Taipei Medical University, Taipei, Taiwan, China;
6Department of Internal Medicine, Landseed Hospital, Pingjen, Taiwan, China.
Email: peterus@hawaii.edu; thajebp@hotmail.com
Received 3 January 2010; revised 12 January 2010; accepted 15 January 2010.
We report on silent brain infarction (SBI) and leuko-
araiosis (LA) of 23 patients with clinically diagnosed
“first-ever” acute ischemic lacunar stroke. The lacu-
nar syndromes were pure motor hemiparesis (10),
pure sensory syndrome (2), ataxic hemiparesis (3),
dysarthria clumsy hand syndrome (3), and sensory-
motor deficit (5). Nineteen out of the 23 patients pre-
sented with completed strokes on arrival to the hospi-
tal, and 4 (17%) developed evolving-stroke within 24
hours of stroke onset. A lacune corresponded to the
acute stroke could be found in all patients on brain
magnetic resonance imaging (MRI), and in 18 (78%)
on brain computed tomography (CT). MRI showed
additional subclinical or asymptomatic “silent brain
infarctions or lacunes” (SBI) in 19 (83%) of 23 pa-
tients, and leuko-araiosis (LA) of moderate to severe
degree (> grade 2) was present in 61% of patients al-
though dementia was absent. Hypertension is the risk
factor in 78% of cases followed by diabetes mellitus,
smoking, and elevated plasma cholesterol level. Inde-
pendence of the types of lacunar syndromes, patients
with hypertension and diabetes mellitus are associated
with high grade LA. None with normal blood pressure
and plasma glucose had grade 3 or grade 4 LA (p <
0.05). In conclusion, evolving-stroke occurs in one-
fifth of patients with “first-ever” lacunar infarct
within the first 24 hours of stroke onset. SBI was
found in 83% of cases. Hypertension and diabetes
mellitus are associated with additional SBI and high
grade LA. The severity of leuko-araiosis per se dic-
tates the cerebrovascular risks.
Keywords: Computed Tomography; First-Ever Stroke;
Lacune; Leuko-Araiosis; Magnetic Resonance Imaging;
MRI; Silent Brain Infarction
Elegant study on 1042 routine autopsied brains by Fisher
in 1965 [1,2], and data from 2,859 necropsied cases re-
ported by Tuszynski et al. [3] suggest that lacunes occur
in between 6% [3] and 11% [1,2] of cases, respectively.
Approximately, eighty percent of these lacunes had no
history of stroke and neurological deficit, and thus called
“asymptomatic” or “silent” lacunes [3,4]. During life,
the diagnosis of asymptomatic or subclinical silent lacu-
nes in the pre-era of MRI has been a difficult task for
several reasons. First, ethically a neurological healthy
subject would not justify having an intensive laboratory
work-up for any possible reason of unexpected intracra-
nial silent lesion. Second, in the earlier days, before the
advent of MRI technique, a brain CT would not sensitive
enough to detect a small lesion of less than 15 mm in a
clinically overt lacunar stroke. Therefore, the actual in-
cidence of subclinical silent lacunes in the general
population, and in asymptomatic patients with cere-
brovascular risk factors remains conjectural. Extensive
use of brain MRI in the past decade had suggested that
prevalence of MRI-based diagnosis of silent brain in-
farction (SBI) ranged from 8% [5] to 28% [6]. These
SBIs included silent lacunes and silent non-lacunar in-
farctions [5-8]. A screening health examination in Japan
on 246 neurologically normal adults revealed 13% had
possible silent lacunar lesions on brain MRI [9]. But
nothing is known about SBI in Chinese/Taiwanese with
“first-ever” acute ischemic lacunar syndromes. This is-
sue will be addressed herein.
Patients recruited in this study were a subset from the
444 P. Thajeb et al. / J. Biomedical Science and Engineering 3 (2010) 443-447
Copyright © 2010 SciRes. JBiSE
authors’ consecutive stroke registry between January 1,
2007 and December 31, 2008. Subjects with a lacunar
infarction due to small penetrating artery occlusion are
often considered “minor” stroke by both laymen and
many clinicians. Good recovery of symptoms and signs
in certain proportion of cases leads to underestimation of
the prevalence of lacunar infarction and silent brain in-
farction. In order to obtain a homogeneous study popula-
tion, we address the question that how often a silent
brain infarction (SBI) can be seen in patients with clini-
cally “first-ever” lacunar stroke? Therefore, patients with
non-lacunar infarction were excluded from the study.
Only those fulfilling all diagnostic criteria set below for
acute first-ever lacunar infarction and those with com-
plete clinical data and available brain CT and MRI
within 5 days of stroke onset will be analyzed. The di-
agnostic criteria of “first-ever” acute lacunar infarction
were: 1) acute stroke with clinical manifestation of one
of the 5 typical clinical lacunar syndromes described by
Fisher [1,2]; 2) absence of past history of presumed
stroke or transient ischemic attack (TIA), including
amourosis fugax; 3) normal electroencephalography
(EEG); 4) neuroimaging studies (brain MRI or CT or
both) showing a corresponded acute brain infarction in
the territory of the penetrating artery and of the size of a
“lacune” (diameter of 15 mm or less); and 5) exclusion
of those with presumed vascular dementia on
mini-mental state examination (MMSE) [10] or modified
mini-mental test (MMT) [11], or both, and on Hatchinski
ischemic score [12]. Twenty-three patients thus recruited
consisted of 6 women and 17 men. The age at stroke
onset ranged from 51 to 85 years (mean 65 years).
MRI was performed by using either one of the fol-
lowing protocol. The old MRI machine (0.5 Tesla su-
perconductive unit, MRI-50 A, manufactured by Toshiba
Corporation) was a multiple-spin-echo T1-weighted im-
age with TR 500 msec/TE 15 msec, T2-weighted images
with TR 3000 msec/TE 120 msec, and proton density
images (PDI) with TR 3000 msec/TE 30 msec. The le-
sions could be round or oval in shape. The single lesion
that matched completely to the clinical presentation (one
of the 5 lacunar syndromes) was called the correspond-
ing lesion. Other unexpected additional (old) lesions or
lacunes were called additional lesions or “silent” lacunes.
A smaller “dot-like”, or spotty high signal intensity on
T2WI and PDI at the cerebal subcortical region that be-
yond the territory of the penetrating arteries, may or may
not be seen on T1WI MRI or brain CT were considered
“etat crible” [13]. The hyperintense poorly demarcated
pathches of irregular border surrounding the lateral ven-
tricles were designated as “leuko-araiosis” (LA) or peri-
ventricular “caps” or “rims” [14]. The grading of sever-
ity of LA was as follows: LA grade 0 (no leuko-araiosis),
LA grade 1 (mild leuko-araiosis at the frontal horn sub-
cortical white matter), LA grade 2 (moderate LA involv-
ing the frontal and posterior horn white matter), LA
grade 3 (severe LA involving the whole rims of lateral
ventricular white matter), and LA grade 4 (advanced LA,
grade 3 LA plus involvement of the centrum semiovale).
The new MRI machine has T1WI [TI 860.0/TR
2,200.0/TE 11.0], T2WI [TR 3,300.0/TE 113.0], FLAIR
[TI 2,500.0/TR 9,000.0/TE 113.0], diffusion weighted
images (DWI) [TR 3,600.0/TE 84.0], ADC map, and
magnetic resonance angiogram (MRA) [TR 37.0/TE 7.0].
MRI definition of a lacune remains the same for T1WI
and T2WI. Additional imaging parameters for acute la-
cunar infarction were lesion of high signal on T2FLAIR,
and DWI, and low signal on ADC map. Asymptomatic
or subclinical “silent” (old) cerebral infarctions were
characterized by signal intensity of iso-or low-signal on
DWI and iso-or high signal on ADC map.
Statistical analyses: Categorical Chi-square or Fisher’s
exact test (for n < 5) were used for statistical analyses.
Probability of < 0.05 was considered statistical signifi-
Mean age at onset was 65 years (range 51 to 85 years)
with men to women ratio of 2.8. There was no statistical
difference between gender and types of lacunar syn-
dromes. Additional lesions suggesting silent cerebral la-
cunar infarctions were encountered in 83% of patients on
MRI (Table 1) as compared to 43% on CT (p < 0.005).
Hypertension was top one risk factor in 78% of patients.
Other risk factors were diabetes mellitus (11 cases,)
(48%), high cholesterol level (> 200 mg/dL) or/and low
HDL-cholesterol level (10 cases), smoking (10 cases),
hyperfibrinogenemia (> 400 mg/dL) (6 cases), high he-
matocrit (4), and hyperuricemia (> 7.5 mg/dL) (4 cases).
The initial manifestations of lacunar syndromes were
pure motor hemiparesis (PMH) in 10 patients, sensoy-
motor deficit (SM) in 5, ataxic hemiparesis (AH) in 3,
dysarthria clumsy hand syndrome (DCH) in 3, and pure
sensory syndrome (PS) in 2. Nineteen of the 23 patients
presented with completed strokes on arrival to the hospi-
tal. Four patients (17%) developed evolving stroke in the
subsequent 24 hours of stroke onset. The frequencies of
abnormalities found on brain CT and MRI were shown in
Table 1. Hyperintense lesions on T2WI and PDI of brain
MRI included the lacunes and etat cribles, were most
commonly encountered at the corona radiata or periven-
tricular white matter (PVWM), followed by internal
Table 1. Frequencies of abnormalities found on brain CT and
MRI of 23 patients with “first-ever” lacunar infarction.
Number (%) of Patients
Detectable abnormalities Brain CT Brain MRI
Corresponding single lesion
of acute infarction 18 (78) 23 (100)
Additional lesions 10 (43) 19 ( 83)*
Leuko-araiosis 2 (9) 14 (61)*
* p < 0.05
P. Thajeb et al. / J. Biomedical Science and Engineering 3 (2010) 443-447 445
Copyright © 2010 SciRes. JBiSE
capsule, basal ganglia, thalamus, and brain stem (Table
2 and Figure 1). Severity of leuko-araiosis in different
subgroups was shown in Table 3. Regardless of the
types of lacunar syndromes, patients with hypertension
or diabetes mellitus were likely having moderate to se-
vere LA (grade 2 to 3) (13 of the 18 patients) (72%, in
contrast to 20% for those without these risk factors).
Combination of hypertension and DM strengthened this
effect from severe to advanced LA (grade 3 to 4). None
of patient with normotension and euglycemia had LA >
grade 2 (p < 0.05).
Table 2. Frequency and locations of additional silent lacunes
and etat crible in 23 patients with various types of acute first-
ever brain lacunar infarctions.
Location of Silent Number (%) of Patients with Positive CT/MRI
Lacunes PMH
Corona radiata* 4 / 7 2 / 3 0 / 1 0 / 21 / 2
Internal capsule 3 / 5 2 / 2 1 / 2 2 / 30 / 1
Basal ganglia 1 / 4 0 / 2 1 / 1 0 / 00 / 0
Thalamus 0 / 2 2 / 3 0 / 1 1 / 11 / 1
Brainstem 1 / 3 0 / 2 1 / 2 0 / 10 / 0
* p < 0.05
Figure 1. (a) Brain CT of an acute lacunar infarction
involving the left thalamus, and old silent lacunes at
left anterior basal ganglion, and right thalamus; (b-e)
Brain MRI of another patient with acute lacunar in-
farction involving the left internal capsule; (b) Diffu-
sion-weighted images (DWI) [TR 3,600.0/TE 84.0];
(c) T1WI; (d) T2WI show additional multiple old
“silent brain infarctions” involving bilateral paraven-
tricular white matter/corona radiata, basal ganglia,
and thalami. MR angiogram; (e) shows mild athero-
sclerotic change with segmental narrowing of the
anterior and middle cerebral arteries (white arrows);
the internal carotid arteries and basilar artery are
relatively normal.
Previous association studies on various risk factors such
as hypertension, diabetes mellitus, cardiovascular dis-
ease, atrial fibrillation, carotid stenosis, and carotid inti-
ma-media thickness, and MRI-diagnosis of silent brain
infarctions (SBI) were contradictory [4,5,9]. Regional
cerebral blood flow in bilateral frontotemporal regions
of brain measured by Xenon-133 inhalation method has
been shown to reduce remarkably in neurologically nor-
mal adults with brain MRI evidence of silent lacunes [9].
But only less than half of the silent lacunes were seen on
T1WI [9]. The autopsied data showed higher (81 %)
frequency of SBI [3]. Recent advance in MRI technol-
ogy improves the detection rate of SBI [4]. SBI was
found more frequently than expected in subjects with no
history of transient ischemic attack or stroke [4]. Hyper-
tension was present in 72% of subjects with SBI [4,6]
that was in accord with our study. Prevalence of SBI
even steeply increases after age of 65 years [4,6-8].
However, hypercholesterolemia, hyperglycemia (fasting
446 P. Thajeb et al. / J. Biomedical Science and Engineering 3 (2010) 443-447
Copyright © 2010 SciRes.
plasma glucose > 110 mg/dL), and high hematocrit (Hct
> 50%) or hypercoagulability were not risk factors of
silent lacunes in several studies, but they were reported
to be risk factors in another study [8,15]. Low-grade
inflammation of cerebral vessel can be another risk fac-
tor of SBI or lacunes [16]. Among 40 patients with la-
cunes, 30% of cases showed single lesion on MRI [17]
and these patients may have neuropsychological abnor-
mality in certain aspect of cognitive domain, even
though cognitive function in general remains normal
[17]. Our data showed that simple neuropsychological
tests such as MMSE, MMT, and Hachinski’s score re-
mained normal in patients with first-ever lacune, regard-
less whether they had or had not SBI [10-12]. A recent
study working on more sophisticated neuropsychological
tests performed at 1 month after acute lacunar infarction
showed that 57.5% of patients had mild cognitive im-
pairment (MCI) that was reflected on lower MMSE
score (mean 28.4) [17]. MMSE score of 28 remains at
the normal range of our healthy controls [11]. Further-
more, Grau and colleagues [17] included subjects with
so called “atypical lacunes” in their study, and this part
constituted more than a half of silent brain lacunes lo-
cated in the striatothalamic region of the brain [17].
Atypical lacunes and pure motor hemiparesis accounted
for most of the subjects with MCI [17]. Thalamic lesion
constituted 44% of PS, 25% of PMH, and 25% of atypi-
cal lacune [17]. Nothing was known about unilaterality
or bilaterality of the thalamic lesion and exact locations
of the involvement of the different thalamic nuclei. A
“typical thalamic lacune” usually located at the lateral
tier of thalamic nucleus and frequently manifested with
PS. However, a medially located thalamic infarction can
be as small as a lacune, either unilateral or bilateral, and
sometimes may be mistakenly considered as a “thalamic
lacune” or an “atypical lacune”. They are actually an is-
chemic stroke involving the paramedian mesencephalic
arteries (PMAS) rather than the deep penetrating arteries
of lacunar infarction [18]. PMAS is a branched or a
trunk disease that frequently manifests itself with cogni-
tive impairment, neurobehavioral dysfunction, and ocu-
lar signs [18]. It is a variant of the top-of-basilar artery
syndrome. Therefore, more delicate test for various do-
mains of cognition and higher brain functions might be
needed to detect trivial abnormality in patients with la-
cunar stroke.
In addition, severe periventricular white matter (WM)
change with higher grade (> 2) of leuko-araiosis corre-
lates with the presence of hypertension (13/18 patients,
in contrast to 1/5 in subjects with normal blood pressure)
(Table 3). This is consistent with the previous studies
[4-7]. Austrian Stroke Prevention Study (ASPS) looking
at a community-based population on elderly normal
subjects over 3-year follow-up [5] have shown that dia-
stolic blood pressure and early-confluent white matter
hyperintensities (WMH) at baseline MRI predicted best
the white matter hyperintensity progression. This was
also confirmed by a 6-year ASPS follow-up study [19].
Moreover, the WMH has been shown to associate with
lower forced expiratory volume in 1 second (FEV1) and
lower income of less than $ 50,000 per year in CHS [6].
WMH progression did not associate with cognitive func-
tioning [5], punctuate WM lesions are considered benign
and not progressive, whereas early-confluent WM ab-
normalities are progressive within 6-year follow-up [19].
This is in contradiction to the CHS study that concluded
that WM findings were associated with impaired cogni-
tive and lower extremity functions [6].
Molecular markers of coagulation activation such as
elevated prothrombin fragment, parameters for endothe-
lial cell damage (thrombomodulin and von Willebrand
factor), and lipoprotein A were significantly higher in
patients with silent lacunes [15]. By contrast, a recently
discovered plasma biomarker, SCUBE1, have been sh-
own to associate with different forms of acute cerebral
infarction and severity of ischemic stroke based on NI-
HSS score. The plasma level of SCUBE1 is remarkably
Table 3. Grading of leuko-araiosis (la) in 23 patients with “first-ever” lacunar infarction, high or normal blood pressure, and high or
normal fasting plasma glucose.
Grade Number (%) of Patients with
Lacunar Syndromes and Positive CT / MRI Associated Risk Factors
LA* PMH (10) SM (5) AH(3) DCH (3) PS (2) HBP(18) NBP(5) HPG(11) NPG(12)
0 ** 7 / 1 2 / 1 2 / 1 1 / 0 1 / 0 0 ** 3 0 ** 3
1 1 / 2 1 / 1 1 / 2 1 / 1 0 / 0 5 1 1 5
2 0 / 3 0 / 1 0 / 0 0 / 0 0 / 1 4 1 2 3
3 1 / 3 1 / 1 0 / 0 1 / 2 1 / 1 7 0 ** 6 1**
4 1 / 1 1 / 1 0 / 0 0 / 0 0 / 0 2 0 ** 2 0 **
*LA: leuko-araiosis; PMH: pure motor hemiparesis; SM: sensorimotor syndrome; AH: ataxic hemiparesis; DCH: dysarthria-clumsy-hand syndrome;
PS: pure sensory stroke; HBP: high blood pressure; NBP: normal blood pressure; HPG: high fasting plasma glucose; NPG: normal fasting plasma
grade 0: absent of LA
grade 1: mild, LA confined to the frontal poles of lateral ventricles (“frontal caps”)
grade 2: moderate, LA confined to the frontal and occipital poles of lateral ventricles (“dual caps”)
grade 3: severe, LA involved the whole lateral ventricles (“dual caps” plus “rims”)
grade 4: advanced, confluent LA lesions surround the centrum semiovale
** p < 0.05
P. Thajeb et al. / J. Biomedical Science and Engineering 3 (2010) 443-447 447
Copyright © 2010 SciRes. JBiSE
elevated in patients with acute infarction due to a trunkor
branched-vessel disease, and slightly elevated or normal
in patients with acute lacunar infarction [20]. Plasma
level of oxidized small dense low-density lipoprotein
(LDL-3) is an independent predictor of silent lacunar
infarction [21].
In conclusion, evolving-stroke occurs in about one-
fifth of patients with “first-ever” acute lacunar infarction
within the first 24 hours of stroke onset. Eighty-three
percent of Chinese/Taiwanese patients with first-ever
lacunar stroke had additional silent brain infarction on
MRI. The presence of both hypertension and diabetes
mellitus predicts the likelihood of high grade leuko-
araiosis and additional SBI. Use of neuroimage studies
in conjunction with scrutinized clinical assessments,
monitoring stroke risk factors, and measurement of cer-
tain molecular or plasma biomarkers may be a future
strategy for early diagnosis and treatment of patients at
risk for silent brain lacunar infarctions.
The authors thank clinicians and technicians that contributed to the
performance of brain CT and MRI examinations. Prof Rossane Harri-
gan is supported by a grant #1R25RR019321 for Clinical Research
Education and Career Development (CRECD) in Minority Institutions;
and Prof Linda Chang is supported by a grant #IU54 NS56883-03 for
Imaging Studies in Neurotoxicity and Neurodevelopment, University of
Hawaii Clinical Specialized Neuroscience Research Program (SNRP).
Conflict of interest: none to declare.
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