Rare disease

CASE REPORT

Calcified embolism: a rare cause of cerebral
infarction
Vijay Chandran, Aparna Pai, Suryanarayana Rao
Department of Neurology,
Kasturba Medical College,
Manipal, Karnataka, India
Correspondence to
Dr Vijay Chandran,
vj_chandran@rediffmail.com

SUMMARY
Calcified cerebral emboli (CCE) are a rare cause of stroke
and these emboli can be identified on a CT scan of the
brain performed for the initial evaluation of stroke. In
this report we present a patient who developed a CCE
following cardiac catheterisation that lodged in the left
middle cerebral artery with resultant right hemiparesis
and aphasia. The calcified embolus was seen on CT but
could not be identified on MRI. Predisposing factors for
CCE include angiography and valve or vessel wall
calcification. The natural history and response to
standard therapy in patients with CCE as compared with
stroke of other aetiologies have not been studied until
now. Increased awareness and ability to identify calcified
emboli will help us to have an improved understanding
of strokes resulting from CCE.

BACKGROUND
Emboli in the cerebral circulation are a common
cause of stroke. Cerebral emboli are most often dislodged material from a thrombus which has formed
either in the heart or in a diseased artery. Rarely,
emboli may consist of materials other than thrombus; such as bits of plaque containing cholesterol
and or calcium, air, fat or tumour fragments.
Calcified cerebral emboli (CCE) are a rare cause of
cerebral embolism and moreover are unique in that
they can be diagnosed with fair certainty from the
initial CT of the brain, which is usually performed
as a first step in the evaluation of a patient with
stroke. Through this case report we would like to
demonstrate how to identify CCE on CT and
discuss the predisposing factors and the possible
implications on therapy that identification of this
condition may have.

CASE PRESENTATION

To cite: Chandran V, Pai A,
Rao S. BMJ Case Rep
Published online: [please
include Day Month Year]
doi:10.1136/bcr-2013009509

An elderly gentleman with no history of hypertension or diabetes mellitus presented with a 2-month
history of angina on exertion. Examination
was normal except for blood pressure of
190/100 mm Hg. His ECG was normal and transthoracic echocardiography (TTE) showed normal
left ventricular function, trivial mitral regurgitation
and mild left ventricular hypertrophy. He underwent coronary angiography for his symptoms; the
procedure was uneventful and showed only mild
coronary artery disease and he was planned for
medical management. Around 6 h after angiography while in the coronary care unit he became
restless, agitated and his speech was found to be
slurred; blood pressure recorded at this time was
200/100 mm Hg, for which he was started on

Chandran V, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-009509

intravenous antihypertensives. The next day
morning on awakening from sleep he had developed dense right hemiplegia, global aphasia with
gaze preference to the left.

INVESTIGATIONS
A plain CT scan of the brain was performed which
showed an evolving hypodensity involving the left
temporoparietal region, a circular hyperdense
lesion in the left sylvian fissure suggestive of a calcified embolism involving the M2 segment of the left
middle cerebral artery (MCA) and calcification of
the wall of the intracranial right internal carotid
artery (ICA; figure 1). MRI with diffusion-weighted
images of the brain performed 1 day after CT confirmed the left MCA territory infarction with
sparing of the basal ganglia consistent with occlusion of the M2 segment (figure 2), however the
MRI itself did not show any signal changes to
suggest a calcified embolism.

TREATMENT
The patient was started on antiplatelets and was
not thrombolysed as he was beyond the window
period.

OUTCOME AND FOLLOW-UP
The patient’s neurological condition remained
status quo, however he developed urinary tract
infection which rapidly progressed to septicaemia.
Despite antibiotic therapy he passed away shortly
thereafter.

DISCUSSION
Intracranial calcifications may be physiological
which include calcifications of the pineal gland,
choroid plexus, basal ganglia and dura mater; or
pathological which include infections either
acquired/congenital, inflammatory lesions, tumours,
phakomatoses, metabolic disorders, dystrophic and
vascular calcification.1 The presence of calcification
in the path of major vessels is suggestive of vascular
calcification2; in the intracranial compartment,
these are most commonly seen involving the
carotid siphon secondary to atherosclerosis.3
Calcification is rarely noted in the MCA or anterior
cerebral artery.3 Calcified emboli may rarely be
seen over the surface of the brain secondary to
being lodged in the superficial smaller arteries.2
The presence of a calcified lesion in the MCA and
resultant ischaemia of the vascular territory distal
to the lesion would suggest that the calcified lesion
was responsible for the neurological deficit in this
patient. Previous reports of calcified cerebral
1

Rare disease

Figure 1 CT of the brain showing calcification of the intracranial right internal carotid artery (A, arrow) and a calcific speck in the left sylvian
fissure corresponding to the M2 segment of the left middle cerebral artery (B, arrow)
embolism have been attributed to angiography,2 4 5 mitral
annular calcification,6 calcified aortic stenosis,7 8 aortic and
carotid vessel wall calcification.2 Our patient developed a calcified cerebral embolism following coronary angiography. His
TTE prior to and after the procedure did not reveal calcification
of the mitral or aortic valve and therefore we believe that the
calcified embolism originated from a vessel wall. No imaging of
the neck vessels was performed as the patient developed other
complications, however brain imaging did show calcification of
the intracranial right ICA suggesting the possibility that he may
have had calcification of other major vessels. The site of origin
of embolism in this case is not evident. One of the possibilities
is embolism originating from the arch of aorta secondary to coronary angiography, the odd feature is the onset of neurological
symptoms several hours after angiography however this has to

be considered in view of the temporal association between the
procedure and the neurological event; another possibility is
spontaneous embolism from the carotid artery in the neck.
Our patient was not thrombolysed as he was outside the
therapeutic window. Current guidelines do not make a distinction between calcified and non-calcified emboli with regard to
thrombolysis. The presence of calcification in an embolus may
play a role in determining the effect of thrombolytic therapy
with some isolated case reports showing a poor response9 10
and others demonstrating a good response.2
These images highlight a rare variety of cerebral embolism
and demonstrate the ability of CT to detect calcified emboli
which would not have been detected by an MRI and thereby
re-emphasises the advantages of CT in the setting of acute
stroke.

Figure 2 Diffusion-weighted images of the brain with left temporoparietal hyperintensity (A) which is restricted on apparent diffusion coefficient
maps (B) suggesting an acute infarct.
2

Chandran V, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-009509

Rare disease
REFERENCES
Learning points

1
2

▸ Calcified cerebral emboli are a rare cause for cerebral
infarction.
▸ Identified by the presence of calcification along the path of
major vessels and rarely over the surface of the brain.
▸ Predisposing factors include cardiac catheterisation, mitral
annular calcification, calcified aortic stenosis and aortic or
carotid vessel wall calcification.
▸ CT is superior to MRI in identifying calcified cerebral emboli.

3
4
5
6

7
8

Contributors All the authors were involved in the conception, design, drafting,
revision and the final approval of the case report.
Competing interests None.
Patient consent Obtained.

9
10

Makariou E, Patsalides AD. Intracranial calcifications. Appl Radiol 2009;38:48–60.
Kavanagh EC, Fenton DM, Heran MK, et al. Calcified cerebral emboli. AJNR Am J
Neuroradiol 2006;27:1996–9.
Sohn YH, Cheon HY, Jeon P, et al. Clinical implication of cerebral artery calcification
on brain CT. Cerebrovasc Dis 2004;18:332–7.
Kirk GR, Johnson JK. Computed tomography detection of a cerebral calcific embolus
following coronary catheterization. J Neuroimaging 1994;4:241–2.
Khaw N, Gailloud P. CT of calcific cerebral emboli after carotid manipulation. AJR
Am J Roentgenol 2000;174:1467.
Konishi-Yakushiji M, Yakushiji Y, Kotooka N, et al. Sonographic confirmation of the
association between calcified cerebral emboli and mitral annular calcification.
J Ultrasound Med 2010;29:1507–10.
Boon A, Lodder J, Cheriex E, et al. Risk of stroke in a cohort of 815 patients with
calcification of the aortic valve with or without stenosis. Stroke 1996;27:847–51.
Rancurel G, Marelle L, Vincent D, et al. Spontaneous calcific cerebral embolus from
a calcific aortic stenosis in a middle cerebral artery infarct. Stroke 1989;20:691–3.
Halloran JI, Bekavac I. Unsuccessful tissue plasminogen activator treatment of acute
stroke caused by a calcific embolus. J Neuroimaging 2004;14:385–7.
Okazaki S, Sakaguchi M, Sugiyama Y, et al. Ineffective thrombolytic therapy for
calcified cerebral emboli originated from calcified internal carotid artery stenosis.
Rinsho Shinkeigaku 2009;49:281–4.

Provenance and peer review Not commissioned; externally peer reviewed.

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Chandran V, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-009509

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