European Journal of Neurology 2007, 14: 937–939

doi:10.1111/j.1468-1331.2007.01762.x

SHORT COMMUNICATION

Lacunar stroke attributable to radiation-induced intracranial arteriopathy
I. S. M. Saliha, N. J. N. Higginsb, E. A. Warburtona and J.-C. Barona
a

Department of Clinical Neurosciences and Stroke Unit, University of Cambridge, Cambridge, UK; and bUniversity Department of

Radiology, Addenbrooke’s Hospital, Cambridge, UK

Keywords:

arteriopathy, lacunar,
medulloblastoma,
radiotherapy, stroke
Received 10 October 2006
Accepted 24 January 2007

We report the rare presentation of lacunar stroke syndrome secondary to single
perforator mouth occlusion from radiation-induced middle cerebral artery (MCA)
stem arteriopathy. A 30-year-old female had acute-onset right-sided ataxic hemiparesis and dysarthria. As a child, she had a medulloblastoma of the posterior fossa and
had surgery followed by cranial radiotherapy. She had no significant vascular risk
factors. Acute CT showed extensive bilateral basal ganglia and left thalamic calcification; DWI showed a left internal capsule lacunar infarct; and MRA and CTA
showed a 50% stenosis of the proximal left MCA.

Stroke can occur as a delayed complication of radiotherapy to the head and neck [1]. Delayed radiationinduced narrowing of large extra-cranial arteries is well
recognized, but intra-cranial arteries can also be involved, e.g. the carotid siphon after radiotherapy for
pituitary or optic pathway tumours [2]. Most cases
reported are large artery syndromes. Very few cases of
single perforator infarct secondary to radiation have
been reported [3].

Case report
A 30 year-old right-handed female presented with
sudden onset slurred speech and right-sided weakness
involving face, arm and leg, with no history of headache, visual impairment or neck trauma. She is a nonsmoker; her father has type-2 diabetes mellitus. There is
no family history of neurological disease. She has no
history of hypertension, diabetes mellitus, cerebrovascular disease, ischaemic heart disease or atrial fibrillation. At age 7 years she was found to have
medulloblastoma of the fourth ventricle and had surgery followed by chemotherapy and radiotherapy. The
tumour was successfully removed without major residual neurological deficit. Post-operatively she received
3500 cGy to the cranium over a 3-week period, 2000 to
the whole spine, and further 1000 cGy to the posterior
fossa. As complications of radiotherapy she had
impaired intellectual development and spine osteoporosis with poor spinal growth leading to short stature.
Clinical examination revealed dysarthria and rightsided ataxic hemiparesis with moderate (3/5 MRC) motor weakness affecting face, arm, and leg equally, with no
Correspondence: Jean-Claude Baron, MD, Department of Clinical
Neurosciences, University of Cambridge, Box 83, Addenbrooke’s
Hospital, Hills Road, Cambridge CB2 2QQ, UK (tel.: +44 (0) 1223586661; fax: +44 (0) 1223-217909; e-mail: jcb54@cam.ac.uk).

Ó 2007 EFNS

sensory impairment. There was no dysphasia or visual
field abnormality, and no extrapyramidal features.
Blood pressure and systemic examination were normal.
CT of the head within 24 h of onset showed extensive
calcification of the basal ganglia and posterior thalamus
bilaterally, but more marked on the left (Fig. 1a). Diffusion-weighted (DWI) 7 days after onset confirmed a
lacunar infarct in the posterior limb of the left internal
capsule, extending to the left putamen (Fig. 1b); its size
did not exceed 1.5 cm in any direction. FLAIR also
demonstrated diffuse white matter changes in the
occipital lobe bilaterally, reflecting damage from radiation (Fig. 1c). She had normal carotid ultrasounds,
transthoracic echocardiogram, 24-h ECG monitoring,
and baseline bloods including fasting glucose, calcium,
phosphorus and alkaline phosphatase; total cholesterol
(TC) was mildly elevated at 6.3 mmol/l with TC/HDL
ratio at 5.3. Auto-immune screen including antiphospholipid antibodies and thrombophilia screen were
negative.
Magnetic resonance angiography (MRA) showed
narrowing and irregular calibre of the whole left middle
cerebral artery (MCA) stem, suggesting local atheroma
(Fig. 1d). These MRA findings were confirmed on CT
angiogram (Fig. 1e); the maximal degree of stenosis was
measured at 50%.
The patient made a good recovery, and was left with
mild right arm weakness and moderate ataxia. She was
started on Aspirin and simvastatin. Her blood pressure
was consistently below 120/80 over 2 years of follow-up.

Discussion
This patient presented with a typical lacunar stroke
syndrome, which is very unusual in young people.
Taken together, the extremely unusual calcification of
the basal ganglia and thalamus on CT; the occipital
lobe white matter changes on FLAIR; the left MCA

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I. S. M. Salih et al.

(a)

(c)

(b)

CT head

DWI

FLAIR MRI

(d)

MRA
(e)

CTA
Figure 1 Imaging findings. (a) CT scan of the head showing bilateral calcifications in the basal ganglia and the posterior thalamus
bilaterally (more marked on the left). (b) Diffusion weighted imaging (DWI) showing high signal in the left posterior limb of internal
capsule and neighbouring lentiform nucleus, consistent with an acute single perforator infarct. (c) FLAIR sequence showing white matter
changes in the occipital lobe bilaterally from childhood radiation therapy. (d) Maximum intensity projection (MIP) MRA of the carotid
system showing narrowing and irregular calibre of stem of the left MCA (arrow). (e) CT angiography (coronal MIP) showing narrowing
and irregular calibre of the stem of the left MCA (arrow).

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Radiation induced lacunar stroke

stem narrowing on MRA and CTA; the young age and
negative young stroke work-up; the lack of vascular
risk factors other than borderline cholesterol; and
finally the history of cranial radiotherapy, strongly
suggest radiation-induced accelerated atheroma of the
left MCA causing occlusion of the mouth of a perforator leading to a single perforator infarct, or, less likely,
of the perforator itself.
The possibility that the basal ganglia calcification
was unrelated to the radiation is very unlikely, as
involvement of the thalamus is very unusual; there was
no known neurological family history; and the patient
had no extrapyramidal features and normal blood calcium. That she had sporadic small vessel disease is also
very unlikely as it is very rare in the young; she had no
vascular risk factor apart from borderline cholesterol;
and her blood pressure was always well within normal
ranges even 2 years down the line, although formal 24 h
monitoring was not performed.
Extracranial disease is well known following radiotherapy to head and neck tumours [1]. However,
involvement of the intra-cranial arteries, especially the
carotid siphon and middle cerebral artery, is also well
documented [3–5]. Huvos et al. documented accelerated
atheroma as the pathological process induced by radiation therapy in large arteries [6].
A lacunar stroke as a consequence of MCA atheroma
causing occlusion of a mouth of a perforator but
unrelated to radiation is well described [7,8], especially
in East Orientals [9] in whom it is the most frequent
presentation of MCA stenosis [10].
Stroke associated with MCA disease caused by
radiation therapy has been reported, though rarely.
Intracranial vasculopathy following radiotherapy for
childhood medulloblastoma has been reported in three
cases [4,5], including one case with extensive basal
ganglia calcifications [5]. Stenosis affected arteries distal
to the Circle of Willis, including one case with >50%
stenosis of the MCA bilaterally [5]. However, neither
case had a lacunar stroke. Bowen and Paulsen [3] described two cases, aged 39 and 46 years, of single perforator infarction occurring 13 and 20 years,
respectively, after pituitary irradiation. In both patients
cerebral angiography revealed stenotic changes in the
internal carotid, but also in the middle and anterior
cerebral arteries in one case, and possibly of the small
perforators in the other case.
Why the radiotherapy given to the posterior fossa
resulted in atheroma localized to the anterior circulation,
and only to the left MCA, is unclear, but the bulk of the
radiotherapy was to the whole cranium, and it is possible
that even the beam angulations for the posterior fossa
were such that the plane of the circle of Willis was involved. The prominent basal ganglia calcification in this

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case (and in a previous similar case [5]) together with the
occipital FLAIR changes would support this idea; whilst
the clear predominance of the calcification on the left
side would fit with the left MCA being mostly affected.
In our case the lacunar syndrome was caused by
perforator occlusion likely secondary to radiation-induced MCA local atheroma. Although the stenosis, as
measured on CT angiogram, was only moderate at
50%, perforator occlusion has been reported in moderate proximal MCA disease [9], e.g. in 50–69% stenosis
[10]. Transcranial Doppler to further document the
stenosis was not performed in our case.
This case-report serves to emphasize that lacunar
syndromes can be due to post-radiation proximal MCA
disease.

Acknowledgements
We thank Dr Justin Cross for his valuable advice on
imaging of this case.

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