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303

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F. Clarençon a,∗
A. Jafari b
M. Lefevre c
S. Périé b
B. Angelard b
C. Marsault a
M. Tassart a
a
Department of radiology, Faculty of Medicine, University
Pierre-et-Marie-Curie Paris-VI, Tenon Hospital, Assistance
publique—Hôpitaux de Paris, 4, rue de la Chine, 75020
Paris, France
b
Department of Otolaryngology-Head and Neck Surgery,
Faculty of Medicine, University Pierre-et-Marie-Curie
Paris-VI, Tenon Hospital, Assistance publique—Hôpitaux de
Paris, Paris, France
c
Department of anatomopathology, Faculty of Medicine,
University Pierre-et-Marie-Curie Paris-VI, Tenon Hospital,
Assistance publique—Hôpitaux de Paris, Paris, France
∗
Corresponding author.
E-mail address: fredclare5@msn.com (F. Clarençon).

Available online 28 April 2009
doi:10.1016/j.neurad.2009.02.006

Arterial spin-labeling demonstrates ictal cortical hyperperfusion in epilepsy secondary to
hemimegalencephaly夽
IRM de perfusion par marquage des spins montrant une hyperperfusion corticale dans un cas
d’épilepsie secondaire à une hémimégalencéphalie
KEYWORDS
Arterial spin-labeling;
Epilepsy;
MRI;
Perfusion

夽 Study supported by the Swiss National Science Foundation (SNF).
Multimodality MR Imaging in tissue characterization SNF 320000121565.

A 5-month-old patient presented with drug-resistant epilepsy in which changes in medication failed to control
seizures. On being referred for pre-surgical evaluation, the
patient received an intravenous injection of 80.17 MBq of
18
F-fluorodeoxyglucose (FDG), 30 min after which integrated
positron emission tomography (PET) and computed tomography (CT) was acquired, using a Biograph 16 (Siemens; Erlangen, Germany). Following CT without contrast enhancement
(2-mm slices) for anatomical co-registration, attenuation
and scatter correction, magnetic resonance imaging (MRI)
was performed, using a 3.0-T Magnetom Trio (Siemens).
Arterial spin-labeling (ASL) was also performed with a
PASL sequence, using the QUIPSII perfusion mode and the following parameters: 16 slices; voxel size: 3.4 × 3.4 × 6 mm;
TA = 5:55 min; lambda = 0.9 mL/g; alpha = 95%; TE/TR/TI1/
TI2/T1(blood3T) (ms) = 15/5000/700/1800/1496,19. Relative cerebral blood flow (RelCBF) maps for ASL were calculated online by the MRI scanner and offline for CEPWI using
Syngo Perfusion (MRI) software. Susceptibility-weighted
imaging (SWI) was performed using 3D acquisition with an
in-plane resolution of 1 × 1 × 1 mm. Diffusion-weighted imaging (DWI) with a 30-directional scan was acquired as well.
MRI demonstrated asymmetry between both hemispheres, with polymicrogyria on the left (Fig. 1). ASL
perfusion showed hyperperfusion in the left parietooccipital regions (Figs. 2 and 3 a, b), while PET/CT showed
enhanced glucose utilization in the left parieto-occipital
lobes (Fig. 3 c—f).
Epilepsy is a common disorder that is generally managed pharmacologically. However, in a number of cases,
simple pharmacological treatment is not sufficient and surgical treatment becomes necessary. Focal lesions can be
detected electrophysiologically and clinically, but may be
localized with greater precision using high-resolution 3D MRI
acquisitions for delineation of anatomical and pathological
structures [1]. In addition, other functional methods, such
as diffusion and perfusion MRI, have been advocated [2,3].
However, in the very young, it may be necessary to use alternative methods to contrast-enhanced perfusion techniques
[4]. One such method is ASL [5], which has been applied
in a number of pathological conditions, especially cerebral
ischemia [6].
In the case of drug-resistant epilepsy, ictal perfusion
changes can be detected by methods such as EEG-triggered
PET, using perfusion or metabolic tracers, and single-photon
emission CT (SPECT), all of which require radiolabeled
compounds. In terms of radiation exposure, MRI perfusion
techniques are less invasive, but also require the use of
contrast. Indeed, recently, there has been concern over the
occurrence of systemic nephrogenic fibrosis with the use
of contrast media. Moreover, due to their inherent working
properties, these conventional contrast-based MRI perfusion
techniques can only reliably demonstrate cerebral blood
flow loss, and not increases.
ASL is a promising non contrast-based brain perfusion
technique that offers the possibility to CBF mapping of the
whole of the brain. While this does not precisely reflect what
we see on PET/CT examination—–which explores metabolism
and not perfusion, as does ASL—–the data do correlate surprisingly well, which may also be because of injection of the
radiotracer close to the occurrence of an epileptic crisis.
This is in agreement with the literature on ASL.

304

Correspondences

Figure 1 Multimodal MRI showing hemimegalencephaly on T2-weighted (a—e), T1-weighted (f—h) and diffusion tensor imaging
(DTI; i, j) scans. There is polymicrogyria on the left as well as reduced anisotropy (i, j).

Thus, while this report only concerns a single case, it
clearly shows that ASL can provide information to support
electrophysiological and nuclear-medicine data regarding
active ictal lesions. In addition, ASL can be safely performed in patients in whom exploration of the brain is
necessary.

References

Figure 2 Arterial spin-labeling perfusion of the brain showing
hyperperfusion of the left parieto-occipital lobes.

[1] Urbach H. Imaging of the epilepsies. Eur Rad 2005;15:494—500.
[2] El-Koussy M, Mathis J, Lovblad KO, Stepper F, Kiefer C, Schroth
G. Focal status epilepticus: follow-up by perfusion- and diffusion
MRI. Eur Radiol 2002;12:568—74.
[3] Heiniger P, el-Koussy M, Schindler K, Lovblad KO, Kiefer C,
Oswald H, et al. Diffusion and perfusion MRI for the localisation
of epileptogenic foci in drug-resistant epilepsy. Neuroradiology
2002;44:475—80.
[4] Wintermark M, Sesay M, Barbier E, Borbély K, Dillon WP, Eastwood JD, et al. Comparative overview of brain perfusion imaging
techniques. J Neuroradiol 2005;32:294—314.
[5] Deibler AR, Pollock JM, Kraft RA, Tan H, Burdette JH, Maldjian JA. Arterial spin-labeling in routine clinical practice, part

Figure 3 Correlation between perfusion methods: ASL (a, b) shows hyperperfusion in the same areas that PET/CT shows enhanced
glucose utilization (c—f).

Correspondences

305

3: hyperperfusion patterns. AJNR Am J Neuroradiol 2008;29:
1428—35.
[6] Altrichter S, Kulcsar Z, Jägersberg M, Federspiel A, Viallon
M, Schaller K, et al. Arterial spin labeling shows cortical
collateral flow in the endovascular treatment of vasospasm
after post-traumatic subarachnoid hemorrhage. J Neuroradiol
2009.

S. Altrichter a
N. Pendse a
M. Wissmeyer b
M. Jägersberg c
A. Federspiel d
M. Viallon e
M. Seeck f
K.-O. Lövblad a,∗
a
Department of Neuroradiology, DISIM,
Geneva University Hospital, 24, Micheli-du-Crest road,
1211 Geneva cedex 04, Switzerland
b
Department of Nuclear Medicine, Geneva University
Hospital, 1211 Geneva cedex 04, Switzerland
c
Department of Neurosurgery, Geneva University Hospital,
1211 Geneva cedex 04, Switzerland
d
Department of Psychiatry, Waldau University Hospital,
3000 Bern cedex 07, Switzerland
e
Department of Radiology, Geneva University Hospital,
1211 Geneva cedex 04, Switzerland
f
Department of Neurology, Geneva University Hospital,
1211 Geneva cedex 04, Switzerland

les crises. L’électro-encéphalogramme objectivait un état
de mal convulsif avec des crises subintrantes continues de
localisation pariétale droite. A.D. était alors transférée
en réanimation pédiatrique où l’hypothèse d’un état
de mal épileptique pharmacorésistant sur malformation
cérébrale était évoquée. Le traitement antiépileptique
a été poursuivi. L’IRM cérébrale a mis en évidence une
prise de contraste piale étendue bilatérale frontopariétale,
prédominant à droite, correspondant à un angiome pial,
avec une atrophie corticale en regard (Fig. 2). Il existait
une hypertrophie des plexus choroïdes (Fig. 3). La présence
d’un angiome leptoméningé a permis de poser le diagnostic
de syndrome de Sturge-Weber. Devant l’absence d’angiome
cutané dans le territoire du V1 ou d’angiome choroïdien, le
diagonstic de syndrome de Sturge-Weber de type III a été
retenu.

∗

Corresponding author.
E-mail address: karl-olof.lovblad@hcuge.ch
(K.-O. Lövblad).
Available online 31 May 2009
doi:10.1016/j.neurad.2009.04.001

Syndrome de Sturge-Weber bilatéral

Figure 1 TDM cérébrale sans injection. Calcifications souscorticales frontales droites. Élargissement des espaces sousarachnoïdiens dans les régions frontales.

Bilateral Sturge-Weber Syndrome

Cas clinique
A.D., âgée de 17 mois, présentant depuis plusieurs jours
une rhinopharyngite et un fébricule, a été hospitalisée pour
un épisode d’hypotonie axiale sans perte de connaissance
suivi de clonies hémicorporelles gauches. L’examen clinique
objectivait un déficit moteur hémicorporel gauche. Les
antécédents de l’enfant étaient marqués par des myoclonies de sommeil de j2 à j21 de vie et un retard des
acquisitions. Le bilan sanguin retrouvait une élévation
isolée des lactates. La ponction lombaire était normale. Le
scanner cérébral sans injection montrait des calcifications
sous corticales frontales droites et des régions centrales
et un élargissement des espaces liquidiens péricérébraux
bifrontaux (Fig. 1). L’évolution n’a pas été favorable sous
traitement anticomitial maximal avec récidive des crises
convulsives partielles à type de myoclonies de la main et
de l’hémiface gauches, sans reprise de conscience entre

Figure 2 IRM cérébrale, coupe axiale pondérée en T1. Atrophie bilatérale dans les régions frontales. Absence d’anomalie
de la gyration.