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Reversible pseudo-tumoral brain
lesion in patient with focal status
epilepticus
An 82-year-old woman, with a past history of epilepsy,
was admitted with 1-week history of aphasia, and a left focal
motor status epilepticus, without fever. Brain MRI (1.5 Tesla
scan), revealed a left subcortical frontal high signal intensity
lesion on FLAIR with low signal intensity on T1WI, without
gadolinium enhancement (Fig. 1A and B).

Despite anti-epileptic treatment, focal status epilepticus remained. A MRI was performed 8 days later showing
an extensive cortico-subcortical fronto-temporal hyperintense lesion on FLAIR (Fig. 1C), with a subarachnoidal
frontal-temporal gadolinium enhancement (Fig. 1D). DWI
and corresponding ADC maps (Fig. 1E and F) demonstrated
high-intense signal without restricted diffusion. A perfusion
MRI (PWI) showed a hyperperfusion of this area.
Laboratory finding including a lumbar puncture, and thoracic, abdominal and pelvis CT scan were normal. Multivoxel
MRI spectroscopy revealed, on the left temporal lesion, a

Figure 1 Axial magnetic resonance imaging (MRI) reveals at day-8 a left subcortical frontal hyperintense lesion in Fluid Attenuated Inversion Recovery (FLAIR) (A) without gadolinium enhancement T1W1 (B). At day-15, before brain biopsy, MRI demonstrates
an extensive cortico-subcortical fronto-temporal hyperintense lesion on FLAIR (C), a subarachnoidal frontal-temporal gadolinium
enhancement (D), and a high signal on DWI (E) without restricted diffusion on ADC (F) corresponding to a vasogenic edema.

http://dx.doi.org/10.1016/j.neurad.2014.10.002
0150-9861/© 2014 Elsevier Masson SAS. All rights reserved.

Please cite this article in press as: Azakri S, et al. Reversible pseudo-tumoral brain lesion in patient with focal status
epilepticus. J Neuroradiol (2014), http://dx.doi.org/10.1016/j.neurad.2014.10.002

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Figure 2 A multivoxel spectroscopy (long TE = 136 ms,
16 × 16, size of voxel 1.1 × 1.1 × 1.5cm3 , Taq = 6 min 8 sec)
shows, on the left temporal lesion a decrease of Nacetylaspartate (NAA), an increase of choline (Cho) and a
negative peak of lactates. The ratios are: Cho/NAA = 2.63,
Cho/Cr = 1.62, NAA/Cr = 0.62. On the right healthy temporal
region, the metabolite spectrum is normal without peak of lactates.

decrease of N-acetylaspartate, an increase of choline and a
negative peak of lactates on a long TE (Fig. 2). Neuropathological analysis of brain biopsy found a gliotic and spongiotic
reshuffle without argument for an inflammatory or tumoral
process.
An aggressive therapy was performed (clonazepam, valproate and phenytoin) with gradual clinical remission 3
weeks later, and normalization of brain MRI (Fig. 3A—B).

Discussion
Striking MRI finding in our case was a development of an
extensive mass involving cortical and subcortical structures

with subarachnoidal frontal-temporal gadolinium enhancement, mimicking an infectious, inflammatory or tumoral
disease.
MRI is an essential investigation in patients with epilepsy
and status epilepticus (SE) for determining the underlying
cause. However, status epilepticus or prolonged seizures
may themselves induce changes in the MRI resulting in difficulty in interpretation [1—4]. Especially, they must be
distinguished from lesions that caused the seizures.
Seizure-induced brain MRI abnormalities are widely
variable, heterogeneous, not necessarily anatomically correlated to the type of epilepsy [2]. They reflect several
physiologic changes such as cerebral edema, hypoxicischemic injury, hyperperfusion and alteration of the
blood-brain barrier [1]. Abnormalities are focal or diffuse,
unilateral or bilateral, involving cortical and/or subcortical
structures, hippocampus, subcortical white matter, basal
ganglia particularly the pulvinar [3,4], corpus callosum, and
cerebellum [2]. A wide range of signal and morphological
characteristics has been reported including: high and lowintensity T2W1 signal, high signal intensity in DWI with or
without focally reduced ADC (cytotoxic rather than vasogenic edema), gadolinium enhancement in cerebral tissue
or in leptomeninges, cortical high signal on T1WI (Laminar
necrosis) [2]. MRI abnormalities may ensure in complete or
partial reversibility [1—4], but it can progress to atrophy [1].
Rarely, as in our patient, the cerebral edema can be
expanded and spread from the cortex to the underlying
white matter, mimicking encephalitis or tumor. As reported
by Szabo et al., the presence of a hyperperfusion on PWI
rules out the diagnosis of a stroke or a progressive multiple leukoencephalopathy [3]. Indeed, hyperperfusion could
be associated with diagnosis such as cerebral lymphoma,
glioma, viral encephalitis, or status epilepticus. Moreover,
here the absence of prior brain MRI studies makes difficult
to distinguish whether the lesion is the cause or the effect of
the seizure. Nevertheless, the result of brain biopsy and the
follow-up brain MRI showing a transient lesion confirm the

Figure 3 Axial FLAIR (A) and contrast-enhanced T1W1 (B) MRI shows recovery of brain MRI abnormalities, after treatment and
clinical resolution.

Please cite this article in press as: Azakri S, et al. Reversible pseudo-tumoral brain lesion in patient with focal status
epilepticus. J Neuroradiol (2014), http://dx.doi.org/10.1016/j.neurad.2014.10.002

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diagnosis of seizure-induced brain MRI abnormalities, which
remains a diagnosis of exclusion.

Conclusion
Increased knowledge of the spectrum of brain MRI may
reduce the risk to mislead the clinical management. Prompt
and aggressive anti-epileptic treatment is necessary to avoid
neuroimaging sequelae.

Disclosure of interest
The authors declare that they have no conflicts of interest
concerning this article.

Acknowledgements
We thank Dr Valérie Rigau, department of clinical pathology,
university hospital center of Montpellier, for performing the
pathological and immunohistochemical examination.

References

3
[2] Cianfoni A, Caulo M, Cerase A, et al. Seizure induced brain
lesions: a wide spectrum of variably reversible MRI abnormalities. Eur J Radiol 2013;82:1964—72.
[3] Szabo K, Poepel A, Pohlmann-Eden B, et al. Diffusion-weighted
and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus. Brain 2005;128:1369—76.
[4] Ohe Y, Hayashi T, Deguchi I, et al. MRI abnormality of the pulvinar in patients with status epilepticus. J Neuroradiol 2014,
http://dx.doi.org/10.1016/j.neurad.2013.09.003.

Souhayla Azakri a,∗
Mahmoud Charif a
Nicolas Menjot de Champfleur b,c
Philippe Gélisse a
Isabelle Mourand a
a
Neurology Department, Montpellier University Hospital
Center, Gui-de-Chauliac Hospital, 80, avenue
Augustin-Fliche, 34295 Montpellier cedex 5, France
b
Neuroradiology Department, Montpellier University
Hospital Center, Gui-de-Chauliac Hospital, Montpellier,
France
c
Team ‘‘Plasticity of Central Nervous System, Stem Cells
and Glial Tumors’’, U1051, Institute of Neurosciences of
Montpellier, Saint-Éloi Hospital, Montpellier, France
∗

[1] Milligan T, Zamani A, Bromfield E. Frequency and patterns of MRI
abnormalities due to status epilepticus. Seizure 2009;18:104—8.

Corresponding author. Tel.: +33 4 67 33 74 13;
fax: +33 4 67 33 79 80.
E-mail address: azsousou@hotmail.fr (S. Azakri)

Please cite this article in press as: Azakri S, et al. Reversible pseudo-tumoral brain lesion in patient with focal status
epilepticus. J Neuroradiol (2014), http://dx.doi.org/10.1016/j.neurad.2014.10.002