Zhou et al. BMC Neurology 2014, 14:16
http://www.biomedcentral.com/1471-2377/14/16

CASE REPORT

Open Access

High-resolution MRI findings in patients with
capsular warning syndrome
Lixin Zhou1†, Jun Ni1†, Weihai Xu1, Ming Yao1, Bin Peng1, Mingli Li2 and Liying Cui1*

Abstract
Background: Capsular warning syndrome (CWS) is rare (1.5% of TIA presentations) but has a poor prognosis
(7-day stroke risk of 60%). Up to date, the exact pathogenic mechanism of CWS has not been fully understood.
We report the clinical presentations and high-resolution MRI (HR MRI) findings of two cases with capsular warning
symptoms.
Case presentation: Case 1 was a 63-year-old man with a history of hypertension with recurrent episodes of left
hemiparesis and dysarthria lasting 10 ~ 30 minutes. Case 2 was a 54-year-old woman with repetitive episodes of
transient left hemiparesis and dysarthria lasting about 10 minutes. Capsular infarctions on DWI were demonstrated
in the territory of a lenticulostriate artery in both 2 patients. HR MRI disclosed atherosclerotic plaques on the ventral
wall of the MCA where enticulostriate arteries were arisen from, although traditional digital subtraction angiography
showed normal. Aggressive medical therapy with dual antithrombotic agents and statin was effective in these two
cases.
Conclusion: Our HR MRI data offer an insight into the pathophysiology of CWS which might be caused by
atherosclerotic plaque in non-stenotic MCA wall. HR MRI might be a useful modality for characterizing atherosclerotic
plaques in the MCA and detecting the pathophysiology of the CWS.
Keywords: Capsular warning syndrome, High-resolution MRI, Middle cerebral artery, Atherosclerotic plaque

Background
The term of capsular warning syndrome (CWS) was first
described in 1993 in patients who presented repeated
stereotyped episodes of subcortical transient ischemic
attacks [1]. It is a popular notion that the syndrome is
associated with a high risk of developing a completed
stroke [2,3]. Up to date, little is known about pathogenic
mechanisms and the role of atherosclerotic disease of
the middle cerebral artery (MCA) in CWS.
A few recent studies have confirmed the feasibility of
using high-resolution magnetic resonance imaging (HR
MRI) to depict the MCA wall and plaques in vivo [4,5].
We report two cases with typical CWS. High-resolution
MRI demonstrated small atherosclerotic plaques on the
ventral wall of proximal MCA, although digital and MR
* Correspondence: pumchcuily@sina.com
†
Equal contributors
1
Department of Neurology, Peking Union Medical College Hospital and
Chinese Academy of Medical Science, Shuai Fu Yuan 1#, Dong Cheng
District, Beijing 100730, China
Full list of author information is available at the end of the article

angiography showed no abnormalities. According to the
findings of HR MRI, possible pathogenic mechanisms of
CWS are discussed.

Case presentation
Case 1

A 63-year-old man with a history of hypertension was
seen with recurrent episodes of left hemiparesis and
dysarthria lasting 10 ~ 15 minutes in the emergency room.
His blood pressure was 136/94 mmHg. Neurological
examination on admission was unremarkable. Treatment
of antithrombotic drug (aspirin 200 mg) and hydration
was given immediately. During the first 48 hours hospitalization he experienced 9 times episodes of left hemiparesis, left central type facial palsy, and dysarthria lasting
13 to 36 minutes. His neurologic status fluctuated between 5 and 11 on the National Institutes of Health Stroke
Scale (NIHSS) and he couldn’t relieve completely after the
last episode with left mild hemiparesis and facial palsy
(NIHSS 3). Brain MRI showed an acute infarct on right
putamen with rostral extension to the corona radiates

© 2014 Zhou et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication
waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise
stated.

Zhou et al. BMC Neurology 2014, 14:16
http://www.biomedcentral.com/1471-2377/14/16

Page 2 of 4

Figure 1 MRI, DSA and HR MRI findings of Case 1. (A) MRI diffusion weighted image shows a hypersensitive lesion on right putamen with
rostral extension to the corona radiates. (B) Digital angiography of the right MCA shows normal. (C) High-resolution MRI of the MCA
demonstrates an atherosclerotic plaque (arrow) on the frontal wall of the right proximal MCA.

Case 2

examination disclosed mild left hemiparesis (grade 4).
Brain MRI demonstrated an acute right-sided infarct on
posterior limb of internal capsular (Figure 2A). Brain
MRA showed no significant abnormalities (Figure 2B).
High-resolution MRI of MCA indicated the presence of
an atherosclerotic plaque on the ventral wall of the right
proximal MCA (Figure 2C). The patient had at least two
episodes of transient left hemiparesis in the emergency
room. Aggressive medical management including a combination of antithrombotic agents of aspirin (200 mg daily)
and clopidogrel (75 mg daily), and statin (atorvastatin
calcium 20 mg daily) was given immediately. The remainder of the patient’s hospital course was uneventful.

A 54-year-old woman developed a sudden onset of left
hemiparesis and dysarthria lasting 10 minutes. After
4 times episodes of transient left hemiparesis in next
4 hours, the patient was admitted to our emergency room.
She denied previous episodes of transient ischemic attack
or stroke. There is no known history of hypertension, diabetes, dyslipidemia, migraine, or heart disease. Her blood
pressure was 170/100 mm Hg on admission. Neurological

Discussion
This is the first study to date on HR MRI findings of
MCA cross-section in patients with CWS. Capsular
infarctions were demonstrated in the territory of a lenticulostriate artery on DWI in both 2 patients. Although
cerebral vascular angiography showed no abnormalities,
HR MRI disclosed atherosclerotic plaques on the ventral

(Figure 1A). A transthoracic echocardiogram revealed no
cardiac source of embolism. Digital angiography of cerebral vascular showed no significant abnormal (Figure 1B).
3-T high-resolution MRI of bilateral MCA demonstrated
an atherosclerotic plaque on the ventral wall of the
right proximal MCA causing the vessel lumen irregular
(Figure 1C). Medical management then switched to a
combination of aspirin (200 mg daily), clopidogrel (75 mg
daily) and statin (atorvastatin calcium 20 mg daily). There
were no more episodes later. The patient was discharged
with mild facial palsy (NIHSS 1) 2 weeks later.

Figure 2 MRI, MRA and HR MRI findings of Case 2. (A) MRI diffusion weighted image shows a hypersensitive lesion on posterior limb of
internal capsular. (B) MR angiography of the MCA is normal. (C) High-resolution MRI of MCA indicates the presence of an atherosclerotic plaque
on the frontal wall of the right proximal MCA.

Zhou et al. BMC Neurology 2014, 14:16
http://www.biomedcentral.com/1471-2377/14/16

wall of MCA where enticulostriate arteries were arisen
from. These HR MRI findings suggested that MCA
atherosclerotic disease may play an important role in
pathophysiology of the CWS in our cases.
The ‘capsular warning syndrome’, a term introduced by
Donnan et al., denotes repetitive transient ischemia
attacks causing stereotyped unilateral motor, sensory, or
sensorimotor deficits that simultaneously affect the face,
arm, and leg without cortical symptoms [1]. CWS is
usually associated with a high risk of capsular infarction
with permanent deficits. A large population-based study
of CWS has found that CWS is rare (1.5% of TIA presentations) but has a poor prognosis (7-day stroke risk
of 60%) [6]. Our two cases both had subsequent capsular
strokes after several episodes of TIAs, which are consistent with previous reports.
The exact pathogenic mechanism of CWS has not been
fully understood. Various mechanisms have suggested,
including small vessel disease, embolism from the heart,
vasospasm, peri-infarct depolarization, and, in rare instances, atherosclerotic disease of the MCA [1,7-10].
Small perforator artery disease is proposed to be the most
common cause of the CWS [1,10,11]. Recently, more
studies suggested that intracranial atherosclerotic disease
plays an important role in the development of small stratiocapsular infarct, especially in Asian [12]. Atherosclerotic plaque of the MCA may occlude the origin of the
lenticulostriate arteries resulting in hemodynamic compromise and subsequent infarct. So we suppose that
artherosclerotic disease of the MCA may be an important
and common pathogenic mechanism of CWS. However,
based on the current traditional imaging technique, little
is known about the role of atherosclerotic disease in the
development of the CWS. Recently, the technique of HR
MRI has been developed to depict intracranial artery wall
in vivo [4,5]. HR MR imaging is able to image a small
plaque that did not yield stenosis on MRA [13,14]. In our
cases, eccentric small plaques on the ventral wall of proximal MCA were identified on HR MRI [15]. Detection of
these small lesions may carry clinical import because a
non-stenostic plaque potentially causes ischemic symptoms via occlusion the origin of the lenticulostriate
arteries. The fluctuating course of stereotyped symptoms
was thought to be the result of hemodynamic compromise
due to the origin occlusion. Relying on the HR MRI findings, we suggest that artherosclerotic disease of the
MCA is an important pathophysiology of CWS.
Different treatment modalities, including hydration,
antiplatelet agents, intravenous thrombolysis and intracranial artery angioplasty, have been proposed in patients with CWS [1,8,9,11,16]. It remains a challenge to
develop therapies that may prevent irreversible damage
to occur in patients with CWS. It seems aggressive medical treatments (including dual antithrombotic agents

Page 3 of 4

of aspirin and clopidogrel, and statin) might be effective
on prevention the recurrent stroke in our cases.

Conclusion
In summary, Our HR MRI data offer an insight into the
pathophysiology of CWS which might be caused from
atherosclerotic plaque in non-stenotic MCA wall. Early
recognition of this clinical presentation and the accompanying stroke mechanism may guide the initial management and prognosis. Further studies using HR MRI in
larger sample subjects are expected for highlighting this
mechanism and guiding the acute treatment decision for
CWS patients.
Consent
“Written informed consent was obtained from the patient
for publication of this case report and any accompanying
images. A copy of the written consent is available for review by the Series Editor of this journal”.
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
LZ and JN were responsible for writing the article. MY was responsible for
collecting case information. ML was responsible for collecting and analyzing
imaging data. WX, BP and LC were responsible for revising the article. All
authors read and approved the final manuscript.
Author details
1
Department of Neurology, Peking Union Medical College Hospital and
Chinese Academy of Medical Science, Shuai Fu Yuan 1#, Dong Cheng
District, Beijing 100730, China. 2Department of Radiology, Peking Union
Medical College Hospital and Chinese Academy of Medical Science, Shuai Fu
Yuan 1#, Dong Cheng District, Beijing 100730, China.
Received: 4 September 2013 Accepted: 15 January 2014
Published: 20 January 2014
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doi:10.1186/1471-2377-14-16
Cite this article as: Zhou et al.: High-resolution MRI findings in patients
with capsular warning syndrome. BMC Neurology 2014 14:16.

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