Brain & Development 26 (2004) 535–538
www.elsevier.com/locate/braindev

Case report

MR imaging and 1H-MR spectroscopy in a case of cerebral infarction
with transient cerebral arteriopathy
Atsushi Imamuraa,*, Naoki Matsuoa, Masako Arikia, Hiroko Horikoshia, Tatsuaki Hattorib
a

Department of Pediatrics, Gifu Prefectural Gifu Hospital, 4-6-1, Noishiki, Gifu 500-8717, Japan
b
Department of Neurosurgery, Gifu Prefectural Gifu Hospital, Gifu 500-8717, Japan

Received 2 September 2003; received in revised form 6 February 2004; accepted 6 February 2004

Abstract
A case of cerebral infarction with transient cerebral arteriopathy in a 12-year-old female is described. The child showed with an acute onset
of left hemiplegia, central facial palsy and aphasia. She was diagnosed with right internal carotid artery obstruction with no predisposing
factors for cerebral infarction. A serial MR image and MR spectroscopy of the brain was performed. MR angiography revealed reversible
vascular changes in the right middle cerebral artery after several months. The ratio of choline/creatine was elevated and that of Nacetylaspartate (NAA)/creatine was depressed in the cerebral lesion, however, they were normalized during the remission phase with long
echo time-MR spectroscopy. The elevation of the lactate peak was clarified with short echo time-MR spectroscopy. The longitudinal follow
up using MR angiography, and MR spectroscopy with long and short echo time was useful for the evaluation of reversible vascular change
with cerebral infarction in children.
q 2004 Elsevier B.V. All rights reserved.
Keywords: Cerebral infarction; Transient cerebral arteriopathy; MR image; MR spectroscopy; Choline; Lactate

1. Introduction

2. Case report

Ischemic cerebral infarction is rare in childhood.
Although the risk factors for childhood stroke include
multiple diseases, such as congenital heart disorders,
cerebral trauma, infection, sickle cell anemia, and metabolic
disorders, no risk factors can be found in 25– 50% affected
children [1]. A recent study revealed that a high proportion
of cerebrovascular disease includes idiopathic cerebral
infarction, termed transient cerebral arteriopathy [2]. We
present a case of cerebral infarction caused by dissection of
the right internal carotid artery of unknown etiology. Serial
MR angiography and MR spectroscopy showed reversible
vascular changes in the arterial lesion. We discuss the
evaluation of neuronal ischemic changes with this patient
using neuroradiological methods.

A 12-year-old girl suddenly demonstrated right occipital
pain after running at school. She was admitted to the Gifu
Prefectural Hospital because of prolonged headache, muscle
weakness developing in her left upper and lower extremities, and presumed global aphasia. She had no significant
medical history, such as congenital heart disease, epilepsy,
or migraines. At the time of the event, she had no preceding
febrile illnesses, and her family history of acute stroke was
unremarkable. Cranial computed tomography (CT) revealed
no marked change, however, hypo-intense and hyperintense lesions in the right middle cerebral artery area
including lacunar areas were shown with T1-weighted and
T2-weighted MR images, respectively. MR angiography
indicated an obstruction in the right terminal tract of the
carotid siphon and the horizontal portion of the right middle
cerebral artery. Cerebral angiography showed a tail-like
narrowing lesion in the right internal carotid artery. The
left MR angiography and cerebral angiography were
normal (Fig. 1). Laboratory findings at admission were
normal, including coagulations test, including prothrombin
time, activated partial thromboplastin time, fibrinogen,

* Corresponding author. Tel.: þ 81-58-246-1111; fax: þ81-58-248-3805.
E-mail address: aimamura30@hotmail.com (A. Imamura).
0387-7604/$ - see front matter q 2004 Elsevier B.V. All rights reserved.
doi:10.1016/j.braindev.2004.02.006

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A. Imamura et al. / Brain & Development 26 (2004) 535–538

Fig. 1. Cerebral angiography (A: right carotid arteriography, B: left carotid arteriography) of the patient with right internal carotid artery obstruction. The arrow
shows a ‘tail-like’ narrowing, a characteristic image for transient cerebral arteriopathy, of the right internal carotid artery. Three-dimensional-time of flight MR
angiography (TR ¼ 27 ms; TE ¼ 3.2 ms, flip angle ¼ 208 (C, D)) and MRI (TR ¼ 3000 ms; TE ¼ 105 ms for T2-weighted (E, F) images) of the patient.
Upper panels (C,E) and lower panels (D, F) represent images obtained at 2 and 6 months after the stroke, respectively. MR angiography revealed reversible
vascular change of the right internal carotid artery at 6 months after the stroke.

antithrombin III, and protein C and S levels. Serum amino
acid analysis including homocysteine, plasma lactate and
pyruvate levels were also normal. Therefore, the patient was
administered low dose aspirin (3 mg/kg/day) to prevent
stroke recurrence, and a rehabilitation program was
initiated. One month later, MR angiography showed
spontaneous regression, however, split dose 131I-IMP single
photon emission CT (SPECT) revealed misery perfusion in
the right middle cerebral artery lesion. Serial MR angiography was performed at 2, 4, 6, and 8 months after the
stroke, and vascular narrowing was no longer detected
(Fig. 1). Electrocardiography and echocardiography were
normal. Localization of a 15 £ 15 £ 15 mm3 region of
interest (ROI) was achieved using long and short TE (250
and 30 ms, respectively) point-resolved spectroscopy
sequences. Proton MR spectra from different ROIs were
acquired within measuring times of 5 min each (TR
2000 ms, 128 accumulations). MR spectroscopy was
performed in two stages, 2 and 6 months after the stroke
attack. MR spectroscopy revealed a low NAA/creatine (Cr)
ratio (1.35; normal at 5– 15 years, 1.80 ^ 0.17) and a high
choline (Cho)/Cr ratio (2.07; normal at 5 – 15 years,
0.89 ^ 0.12) [3,4] with long TE in the ishemic lesion at
the earlier stage (Fig. 2). The ratios of NAA/Cr and Cho/Cr
were nearly normalized at a later stage, 1.76 and 1.37,
respectively. The NAA/Cho ratio improved from 0.65 to
1.28 after 4 months of treatment (Fig. 3). The lactate peak

was elevated in the lesion with short TE, however, it was
unclear with long TE MR spectroscopy in both stages (Figs.
2 and 3). Her headache and aphasia improved within a few
days, however, the mild left hemiplegia remained.

3. Discussion
Ishemic cerebral infarction is rare in childhood. In a
previous study, the frequency, excluding children with
sickle cell disease, was less than 1 in 100,000. Although
the etiology was unknown in the present patient,
arteriopathic stroke is the most common cerebral
infarction in children [1,5]. Cerebral arteriopathy is
characterized by the following two characteristics: first,
subcortical infarcts, such as basal ganglia and internal
capsule, associated with lesions of the cerebral arterial
wall are mostly located in the initial parts of the basal
arteries of the carotid system, and second, clinical and
angiographic follow up should demonstrate a regression
or arrest of the evolution of the arteriopathy [2,5]. In the
present patient, a tail-like narrowing lesion in the
proximal portion of the right internal carotid artery
without string-bead signs, indicating fibromuscular dysplasia, was revealed in the early stages of the stroke by a
cerebral angiogram [2,6], and reversible vascular changes
were shown with serial MR angiography and SPECT.

A. Imamura et al. / Brain & Development 26 (2004) 535–538

537

Fig. 2. Proton MR spectroscopy with short TE (30 ms: A, B) and long TE (250 ms: C, D) localized on the bilateral corpus striatum at 2 months after the stroke.
That of the right lesion (solid square: A, C), which revealed T2 elongation on MRI, showed a peak lactate level at 1.3 ppm of the chemical shift with short TE,
and increased Cho/Cr (2.07) and decreased NAA/Cr (1.35) with long TE. That of the left (dotted square: B, D) showed normal Cho/Cr (1.07) and NAA/Cr
(2.39) ratios.

Fig. 3. Proton MR spectroscopy with short TE (30 ms: A, B) and long TE (250 ms: C, D) localized on the bilateral corpus striatum 6 months after the stroke.
That of the right lesion (solid square: A, C) also showed a lactate peak with short TE, however, the ratios of Cho/Cr and NAA/Cr improved to 1.37 and 1.76,
respectively. That of the left (dotted square: B, D) indicated Cho/Cr and NAA/Cr as 1.31 and 2.69, respectively.

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A. Imamura et al. / Brain & Development 26 (2004) 535–538

Inflammatry episodes, such as varicella zoster infection,
were not shown. These findings suggest that the stroke
may have been caused by transient cerebral arteriopathy
of unknown origin as described by Chabrier et al. [2,5].
In the MR spectroscopy with long TE, low NAA/Cr and
high Cho/Cr ratios were shown in the early stages after
the stroke. NAA is located almost exclusively in neurons
and axons, therefore, NAA is reduced in ischemic
neuronal processes. NAA is degraded by enzymes within
the injured neurons in the first few days or hours after
infarction. Cho appears to contain contributions from
phosphorylcholine and glycerophosphorylcholine, which
are precursors to the cell membrane and breakdown
products of the cell membrane, respectively. Therefore,
an increased Cho signal may reflect membrane degradation after cell lysis and is suggested to be an indicator
of active demyelination [7,8]. These ratios were almost
normalized in the later stages after the stroke. In
addition, the qualitative measurement of regional cerebrovascular reactivity to acetazolamide using split dose
131
I-IMP SPECT suggests the acetazolamide-enhanced
vasoreactive perfusion of the right middle cerebral artery
lesion recovered from 24% in the early stages to 70% at
6 months after the stroke (data not shown). These
findings suggest that the neurons in the ischemic lesion
were not functional but nevertheless still viable, so
called, penumbra [9]. The increased NAA/Cr and
decreased Cho/Cr ratios along with the improvement in
cerebral perfusion suggest recovery of the neuronal cells
and terminated demyelination processes in the ischemic
penumbra. On the other hand, the lactate peak in MR
spectroscopy was not shown with long TE, but was
visible with short TE. Lactate is an indicator of
anaerobic metabolism. In a previous MR spectroscopy
study of patients with cerebral infarction, only the lactate
signal was shown in the irreversible chronic ischemic
tissue, however, multiple peaks including NAA, choline,
creatine and lactate were detected in the ishemic
penumbra [10]. Proton MR spectroscopy with short TE
has the advantage of detection of additional metabolites
with short T2-relaxation times, such as mobile lipids,
proteins, myoinositol, glucose, glutamate, and glutamine
[4,8]. Therefore, lactate including mobile lipids may be
shown only in MR spectroscopy with short TE, nevertheless, other metabolites were detected with long TE in
the present patient. There is no clear correlation between
the metabolites of the acute stage of stroke and clinical
outcome [7], therefore, further evaluation will be
necessary to elucidate the prognostic potential of MR
spectroscopy in childhood stroke.

In this study, we examined a patient with occlusion of the
right internal carotid artery with transient cerebral arteriopathy. Dissection of the artery was reversible and the
clinical course of the patient was very good after treatment.
Clinical improvement with relation to neuroimaging findings was unclear in our patient, however, the serial follow
up using MR angiography and MR spectroscopy with long
and short echo time was useful to evaluate the neuronal
tissue for reversible vascular change with cerebral infarction
in children.

Acknowledgements
We thank Shinichi Yoshimura, MD, Department of
Neurosurgery, Gifu University School of Medicine, for the
study of split dose 131I-IMP SPECT.

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