symptoms. Prevalence of silent brain infarcts (8%–28%)
increases with age and is higher in those with a history of stroke
or dementia.1–3 Presence of silent brain infarcts increases risk
of subsequent stroke and significantly increases the risk of
cognitive impairment.4,5 Cardiovascular risk factors known to
increase the risk of stroke are also associated with silent brain
infarcts1; thus, timely institution of preventive treatment strat-
egies in individuals with “silent strokes” may be critical for
reducing risk of subsequent stroke and dementia.
Classification of strokes as “silent” is based on recall of neu-
rological stroke- like symptoms or transient ischemic epi-
sodes by the patient. However, symptoms may be forgotten or
ignored, especially in patients with cognitive impairment or
social isolation, thus delaying or escaping medical attention.
We report incidentally detected acute and subacute strokes
and examine whether they were truly asymptomatic.
nfarcts are classified as “silent” when they are detected on
brain imaging but lack temporally correlated stroke- like
We collated imaging and clinical data from subjects recruited in MRI
studies at the Memory Ageing and Cognition Center of the National
University Health System, Singapore. Informed consent was obtained
from each subject. Data on demographics and medical history (includ-
ing history of cerebrovascular events) was obtained, clinical assess-
ment performed, and a validated neuropsychological battery (Vascular
Dementia Battery)6 administered for determining cognitive status.
MRIs were performed at the Clinical Imaging Research Centre
on a 3-T Siemens Magnetom Trio Tim scanner. Imaging proto-
col included T1- and T2-weighted, diffusion- weighted imaging,
apparent diffusion coefficient, fluid- attenuated inversion recovery,
susceptibility- weighted imaging, and MR angiography. Hyperintense
lesions on diffusion- weighted imaging with corresponding hypoin-
tense areas on apparent diffusion coefficient were defined as acute/
subacute ischemic stroke. Lesions were labeled “incidental” (IHDWI)
if subjects, or their families, did not voluntarily report symptoms or
seek medical attention.
Background and Purpose—The prevalence of silent brain infarcts varies from 8% to 28% in the general elderly population.
Silent brain infarcts are associated with increased risk of subsequent stroke and cognitive dysfunction. By definition,
silent strokes lack clinically overt stroke- like symptoms and fail to come to clinical attention; however, impaired recall
of symptoms may be a potential confounder. Our aim is to report a series of patients with incidentally detected acute and
subacute strokes and examine whether they were truly asymptomatic.
Methods—Subjects included in this study were drawn from ongoing dementia research studies at the Memory Ageing
and Cognition Center, in which all participants underwent a cranial MRI. Incidental hyperintense lesions on diffusion-
weighted imaging with corresponding apparent diffusion coefficient defects indicative of acute/subacute silent stroke
were identified. Clinical data for individuals with incidental hyperintense lesions on diffusion- weighted imaging were
Results—Six of 649 subjects had incidental hyperintense lesions on diffusion- weighted imaging; on retrospective questioning,
3 recalled symptoms temporally correlated with MRI lesions, which had been reported to but ignored by family members.
Two subjects had focal neurological signs. A majority of the subjects with incidental hyperintense lesions on diffusion-
weighted imaging had significant cognitive impairment.
Conclusions—A significant number of strokes may be “silent” due to lack of awareness of stroke- like symptoms in the
elderly and their families. Enhanced stroke prevention education strategies are needed for the elderly population and, in
particular, for their families. (Stroke. 2012;43:3102-3104.)
Key Words: acute stroke ◼ asymptomatic diseases ◼ diffusion-weighted imaging
Not Listened to Rather Than Silent
Monica Saini, MD; Kamran Ikram, MD, PhD; Saima Hilal, MBBS; Anqi Qiu, PhD;
Narayanaswamy Venketasubramanian, FRCP; Christopher Chen, FRCP
Received June 19, 2012; final revision received July 11, 2012; accepted July 25, 2012.
From the Departments of Pharmacology (M.S., S.H., C.C.), Ophthalmology (K.I.), Bioengineering (A.Q.), NUS, Singapore; the Clinical Imaging
Research Centre, National University of Singapore, Singapore (A.Q.); and the. Division of Neurology, University Medicine Cluster, NUS, Singapore
Correspondence to Christopher Chen, FRCP, Department of Pharmacology, Building MD11 Level 5, Medical Drive, NUH, Singapore 117597. E-mail
© 2012 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.112.666461
Saini et al Silent Stroke 3103
Over a period from August 2010 to May 2012, 649 subjects
underwent an MRI. One hundred forty- six subjects (22.4%)
had evidence of nonacute infarcts; 77 (11.8%) did not give any
clinical history of stroke or transient ischemic attack. IHDWIs
were seen in 6; demographic and clinical characteristics of
these individuals are tabulated (Table 1). Mean age of subjects
with IHDWI was 79.3±4.6 years. All subjects with IHDWI
had ≥1 vascular risk factors; none had a history of clinically
Characteristics of IHDWI and associated MRI features
are presented (Table 2; Figure). Five IHDWIs were sub-
cortical; one was at the gray–white junction. Five subjects
with IHDWI had significant white matter disease (Fazekas
scale),7 and 4 had multiple microbleeds. Neuropsychological
assessment revealed significant cognitive impairment in 5; 4
were diagnosed as CIND–moderate (cognitively impaired,
not demented) and one fulfilled Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition criteria for
Subjects with IHDWI were interrogated specifically for
stroke- like and other symptoms on the day or in days pre-
ceding MRI. In 3 subjects, acute- onset symptoms (interval
from MRI 0–4 days) had been reported to or noted by the
families. However, symptoms were dismissed as not requir-
ing medical attention. In 2, the symptoms were regarded as
part of ongoing cognitive impairment; in another, ataxia was
attributed to “confusion.” Three subjects did not recall any
symptoms. One subject (ID 1) with no history of stroke- like
symptoms had focal neurological signs, which may have
been secondary to an earlier “silent stroke” (old cerebellar
All subjects were referred to emergency care services for
hospital admission; however, one subject declined further
medical evaluation. Appropriate treatment modifications
(addition of antiplatelet medication, statins) were made for
the other 5 subjects during their hospital stay.
Silent brain infarcts differ from symptomatic strokes in that
they lack stroke- like symptoms and fail to reach medical atten-
tion; their prognostic implications are significant in terms
of serving as biomarkers for risk of subsequent stroke and
dementia.4,5 Although the prevalence of silent brain infarcts
has been reported in various studies, data on presence of
“silent” acute/subacute diffusion- weighted imaging lesions
are scarce. Yamada et al8 reported incidental acute infarcts
in 0.37% of their study population undergoing MRI in a
Table 1. Characteristics of Subjects With IHDWI
ID Sex Age, y Vascular Risk FactorsSymptomsSigns
1 Male78 HT, DM, IHD
Chronic renal failure
HT, DM, dyslipidemia, IHD
None Left upper limb ataxia
2 Female85 None None
Left lower limb clumsiness 4 d previously
Lethargic for 2–3 d
5 Male73Imbalance at the time of walking for a
Gait ataxia; confusion;
left upper limb apraxia
None6 Male 81HT, IHD
IHDWI indicates incidental hyperintense lesions on diffusion- weighted imaging; HT, hypertension; DM, diabetes mellitus; IHD, ischemic heart disease.
Table 2. MRI Features in Subjects With IHDWI
White Matter Disease
IDPV DWM Chronic Lacune IHDWI Characteristic Microbleeds Intracranial Stenosis
122 Cerebellar Left parietal deep subcorticalBasal ganglia, thalamus,
subcortical, brain stem, cerebellar
Thalamus and subcortical
Basal ganglia, thalamus,
deep white matter, cerebellar
Cerebellum, pons, bilateral
Left vertebral, right ICA
Right parietal subcortical
Right parietal, subcortical
Right parietal deep subcortical
Right splenium and caudate
Right parietal, gray–white
Right MCA; basilar, left vertebral
Right MCA, right vertebral
…622 Right vertebral
IHDWI indicates incidental hyperintense lesions on diffusion- weighted imaging; PV, periventricular; DWM, deep white matter; ICA, internal carotid artery; MCA,
middle cerebral artery; intracranial stenosis, ≥50% reduction in vessel lumen; chronic lacune, hypointense fluid- attenuated inversion recovery lesion >2 mm, with
3104 Stroke November 2012
hospital- based setting, for a large variety of indications,
including a recent stroke; however, data regarding tempo-
rally correlated symptoms were not collected.. Incidental
acute diffusion- weighted imaging lesions have also been pre-
viously reported in patients of cerebral autosomal- dominant
arteriopathy with subcortical infarcts and leukoencepha-
lopathy (CADASIL); 49% of these patients had acute hem-
orrhages and 15% had chronic memory loss or nonspecific
The “silence” of stroke has been attributed to occurrence
in clinically ineloquent areas. However, we observed that
the “silence” was also attributable to symptoms and signs
being ignored. Although subjects reported symptoms, neu-
rological and otherwise, to caregivers, they were not deemed
to be significant. The majority of subjects with IHDWI had
significant cognitive impairment, and it is possible that this
may have played a role in underrecognition of symptoms,
inability to specify character of deficit (lethargy), or reduced
Five subjects with IHDWI had significant white matter
disease and 2 had evidence of old lacune(s). It has been
shown previously that almost 30% of lacunar infarcts do
not cavitate.10 Thus, if imaged in the chronic phase, almost
one third of patients with lacunar strokes may, in fact,
escape medical attention. Control of vascular risk fac-
tors and prevention of stroke are critical for minimizing
the development and progression of cognitive impairment
and dementia. The profiles of our subjects with incidental
acute strokes underline the urgent need for sensitizing fami-
lies and caregivers of the elderly regarding recognition of
stroke- like symptoms.
Sources of Funding
Memory Ageing and Cognition Center studies are funded by National
Medical Research Council (NMRC) Grant no. R-184–006–184–511.
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Figure. IHDWI; single (A) and multiple (B) DWI
lesions; single DWI lesion (C) with matched ADC
defect (D; arrow). IHDWI indicates incidental hyper-
intense lesions on DWI; DWI, diffusion- weighted
imaging; ADC, apparent diffusion coefficient.