A case of paradoxical brain embolism presenting as a typical lacunar stroke

doi:10.4236/health.2011.34044

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Vol.3, No.4, 249-252 (2011) Health

doi:10.4236/health.2011.34044

A case of paradoxical brain embolism presenting as a

typical lacunar stroke

Gian Paolo Anzola1*, F. Casilli 2, E. Onorato2

1Service of Neurology, S.Orsola Hospital FBF, Brescia, Italy; *Corresponding Author: gpanzola@numerica.it

2Department of Cardiology, S.Orsola Hospital FBF, Brescia, Italy.

Received 18 November 2009; revised 8 January 2010; accepted 15 January 2010.

ABSTRACT

A 59 year old white male presented with a clini-

cal picture typical of lacunar stroke. However, a

thorough diagnostic work up showed that the

most probable mechanism of stroke was para-

doxical brain embolism through a patent fora-

men ovale. The clinical-neuroradiological mis-

match that ultimately lead to the correct inter-

pret ation is discussed.

Keywords: Lacunar Stroke; Patent Foramen Ovale

1. INTRODUCTION

Lacunar strokes are usually recognizable on clinical

grounds when one of the “typical” clinical presentations

identified by Mille-Fisher [1] is coupled with the lack o f

obvious cardiac embolic sources or major atherosclerotic

lesions of the supplying vessels. Conventional neuroi-

maging (CT scan or T2 weighted MRI) is considered

useful to exclude non vascular lesions, but with little

additive value in identifying the cause of stroke.

We report a case of an apparently typical lacunar

stroke in whom, on the contrary, Diffusion Weighted MRI

was of paramount importance in suggesting the correct

cause.

2. CASE REPORT

A 59 year old male caucasian craftsman was admitted

with a two day history of right sided weakness of sudden

onset, difficulty with walking, but no change in con-

sciousness, headache, subjective visual complaints, or

cutaneous sensory symptoms.

He had a history of long standing non insulin de-

pendant diabetes and hypertension. Two years earlier he

had sustained transient numbness and loss of strength

affecting his left arm and lasting for some days.

On admission he appeared fully alert and aware. He

had no aphasia, visual field defects, or dysphagia, and a

barely appreciable slurring of speech with right sided

mild hemiparesis (arm drift and slow leg fall) sparing his

face. There was no sensory disturbance.

Arterial blood pressure was 160/90, EKG showed si-

nus rhythm.

Routine blood tests revealed total cholesterol 220

mg/dl, blood sugar 143 mg/dl, creatinin 0,8 mg/dl, D-

Dimer > 600 ng/ml (normal < 275 ng/ml ).

Echo Doppler disclosed only minimal narrowing of

carotid walls, transcranial Doppler > 20% asymmetry

with reduced mean flow velocity in th e left middle cere-

bral artery. Transthoracic echocardiograph y show ed mild

left ventricular hypertrophy.

The clinical picture of pure motor brachio-crural

hemiparesis ( with no “cortical” features) in conjunction

with diabetes and hyperten sion in the absence of signifi-

cant carotid disease and no obvious potential cardiac

sources of embolism led to the provisional diagnosis of

lacunar stroke. A neuroimaging procedure was then per-

formed.

T2 weighted FLAIR MRI showed multiple spot like

lesions affecting the basal ganglia, the internal capsule

and the white matter of the corona radiata bilaterally,

which seemed to confirm the diagnosis of small vessel

disease. However, DWI sequences, besides showing a

bright spot in the posterior limb of the left internal cap-

sule, which was probably responsible for the clinical

pictures also disclosed a number of further recent lesions

scattered in the subcortical and deep white matter of

both hemispheres, compatible with multiple microem-

bolic occlusions of perforati n g vesse l s.

Following MRI, it was decided to proceed to in-

tra-arterial arteriography, which ruled out significant

lesions of the aortic arch and the intracranial cerebral

arteries.

A Doppler study of lower limbs revealed very minor

irregularities of the calf veins with no evidence of overt

thrombosis. A transcranial bubble test showed a right-

to-left shunt with 30 bubbles in basal conditions and

>100 with curtain pattern following Valsalva strain.

A. GP et al. / Health 3 (2011) 249-252

250

(a)

(b)

Figure 1. T2 FLAIR MRI showing multiple spotlike

lesions in the basal ganglia, internal capsule and thala-

mus (panel A). In the hemispheric white matter the ab-

normalities tend to become confluent (panel B).

This finding, together with the elevation in plasma

D-dimer, the results of venous Doppler and the appear-

ance of DWI MRI, were considered compatible with

brain paradoxical embolism through a patent foramen

ovale. During the entire hospital stay continuous ECG

telemetry revealed no significant abnormality.

Because of the diffuse white matter abnormalities, and

the history of diabetes and hypertension, long term oral

anticoagulation was deemed unsafe. Therefore, one month

later following a short course of low molecular weight

heparin, the patient underwent a successful transcatheter

closure of the patent foramen ovale with a Cardia In-

trasept device. He has since fared well and at one year

follow up he has resumed his job with only mild clum-

siness in the finger movements of his right hand.

3. DISCUSSION

This case had a presentation typical of a lacunar syn-

drome, entailing a pure motor stroke in a hypertensive,

diabetic patient without obvious arterial or cardiac em-

bolic sources. The lacunar hypothesis, as put forward by

Miller-Fisher, assumes that specific clinical syndromes

are produced by infarctions in the territory of a single

perforating artery at the base of th e brain or in the brain-

stem as a consequence of local phenomena such as lipo-

hyalinosis or microatherom a [1] .

With the advent of CT and MRI neuroimaging since

the beginning of the ‘90s [1,2], the first part of the hy-

pothesis was shown to be substantially correct whereas it

proved much more difficult to demonstrate the second

part. About 10% of lacunar syndromes are due to non

ischemic brain damage [3], but even when the underly-

ing pathological cause is ische mic it has proved difficult

to identify a single mechanism. The traditional common

teaching of local occlusion promoted by diabetes and

hypertension is not supported by epidemiological evi-

dence, as hypertension and diabetes are no more com-

mon in lacunar than in non lacunar strokes [4-6]. On the

other hand, Miller Fisher himself admitted and postu-

lated that some of his cases might have been due to em-

bolism, mainly on the basis of the patency of th e arteries

supplying the infarcted tissue [1]. Therefore, even in

recent textbooks [7] the precise etiological interpretation

remains doubtful, although it is often suggested that car-

diogenic embolism is a very rare cause of lacunar syn-

dromes [2,4,5]. Contrary to this assumption Wessel et al.,

by systematically investigating patients with DWI- MRI,

found that 14 (19%) out of 73 patien ts with lacunar syn-

dromes had multiple recent lesions in different areas,

thus suggesting cardiac embolism as the likely cause [8],

although they only rep orted atrial fibrillatio n as potential

embolic source in 3 patients. More recently Ueno et al.

[9] included RLS as a potential cardiac source of emboli

and found that compared with the 32 % prev alence found

in healthy controls, lacunar patients had a significantly

higher 41% prevalence when hypertension and/or diabe-

tes were present and a still higher 82% prevalence when

neither risk factor was present. However they did not

correlate the presence of RLS with the MRI findings [9].

In the present case, we were able to demonstrate both

the embolic nature of the stroke and the underlying

mechanism. Despite the presence of both hypertension

and diabetes the finding of a massive shunt associated

with the elevation of D-dimer, the abnormalities of ve-

nousechography and the lack of arrhythmia are highly sug-

A. GP et al. / Health 3 (2011) 249-252

2512

(a) (b) (c)

Figure 2. DWI MRI showing multiple recent bright lesions in the left posterior internal capsule (arrow, panel (a)) and bilat-

eral hemispheric white matter (arrows, panels (b) and (c)).

gestive of paradoxical brain embolism (PBE) as the most

probable explanation of the embolic pattern seen on

MRI.

PBE is considered a likely cause of stroke in young

patients when more common causes are excluded. How-

ever, it can be important also in older patients [10] and

as an independent factor even when other cerebrovascu-

lar risk factors are present [11].

Therefore, since patent foramen ovale can be found in

as many as 25% of stroke patients with essentially no

specific clinical profile [12], PBE should be considered

within the differential diagnosis even when apparently

more obvious alternative diagnoses are contemplated,

once DW-MRI has suggested the presence of an embolic

ischemic pattern.

In conclusion, this case highlights on one hand the

low predictive value of the clinically defined lacunar

picture in identifying the cause of the stroke and on the

other hand the usefulness of the systematic application

of the most recent techniques of neuroimaging. In fact it

was the MRI appearance that pointed towards a system-

atic search for embolic sources that would probably have

otherwise bee n overl oo ked.

4. Acknowledgement

The Authors wish to thank Dr Edward Stonehill for his friendly co-

operation in improving the text an d revising the English.

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