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Radiología. 2012;54(1):9---20

www.elsevier.es/rx

UPDATE IN RADIOLOGY

Structural magnetic resonance imaging in epilepsy�

J. Álvarez-Linera Prado

Sección de Neurorradiología, Hospital Ruber Internacional, Madrid, Spain

Received 27 December 2010; accepted 9 July 2011

KEYWORDSMagnetic resonance;Epilepsy;Mesial temporalsclerosis;Focal corticaldysplasia

Abstract Magnetic resonance imaging is the main structural imaging in epilepsy. In patientswith focal seizures, detection (and characterization) of a structural lesion consistent with elec-troclinical data allows therapeutic decisions without having to resort to other more expensive orinvasive diagnostic procedures. The identification of some lesions may provide prognostic value,as in the case of Mesial Temporal Sclerosis (MTS) or may contribute to genetic counseling, as inthe case of some Malformations of Cortical Development (MCD).

The aim of this paper is to review the current state of structural MRI techniques, proposea basic protocol of epilepsy and mention the indications for structural MRI and also, reviewthe semiology of the main causes of epilepsy, with emphasis on MTS and MCD, by its highestfrequency and by the special impact that MRI has shown in dealing with these entities.© 2010 SERAM. Published by Elsevier España, S.L. All rights reserved.

PALABRAS CLAVEResonanciamagnética;Epilepsia;Esclerosis temporalmedial;Displasia corticalfocal

Resonancia magnética estructural en la epilepsia

Resumen La resonancia magnética (RM) estructural es la principal técnica de imagen en laepilepsia. En pacientes con crisis focales, detectar (y tipificar) una lesión estructural congruentecon los datos electroclínicos permite tomar decisiones terapéuticas sin necesidad de acudir aotros medios diagnósticos más costosos o invasivos. La identificación de algunas lesiones aportavalor pronóstico, como en el caso de la esclerosis temporal medial (ETM), o puede ayudar alconsejo genético, como en el caso de algunas alteraciones del desarrollo cortical (ADC).

El objetivo de este trabajo es revisar el estado actual de las técnicas de RM estructural y

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proponer un protocolo básico de epilepsia, así como mencionar las indicaciones para realizaruna RM estructural. También se revisará la semiología de las principales lesiones que causanepilepsia, como la ETM y las ADC, por su mayor frecuencia y por el especial impacto que la RM
estructural ha demostrado en su© 2010 SERAM. Publicado por El
� Please cite this article as: Álvarez-Linera Prado J. Resonancia magné2012;54:9---20.

E-mail address: [email protected]

2173-5107/$ – see front matter © 2010 SERAM. Published by Elsevier Esp

diagnóstico y tratamiento.sevier España, S.L. Todos los derechos reservados.

tica estructural en la epilepsia. Radiología.

aña, S.L. All rights reserved.

dx.doi.org/10.1016/j.rxeng.2011.07.001

http://www.elsevier.es/rx

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ntroduction

he study of the structure and function of the brain is anssential step for the diagnosis of patients with epilepsy.tructural magnetic resonance imaging (MRI) is the imag-ng technique that provides the most relevant informationn the diagnostic and therapeutic process of these patients.owever, this information largely depends on choosing anppropriate protocol able to provide suitable spatial resolu-ion and signal-to-noise ratio, as well as optimal gray---whiteatter contrast. Any damage to the cortical gray matter of

he cerebral hemispheres may cause epilepsy. Topic-specificiterature should be consulted for more detailed informa-ion. Mesial temporal sclerosis (MTS) and focal corticalysplasia (FCD) are the most common causes of refractoryocal seizures, and they will therefore be discussed in detail.

MRI contributes to determine the possible focal origin ofome seizures as well as the postoperative outcome---moreavorable in conditions such as MTS, glial tumors or vascularalformations, these latter with a surgical success rate of

0---90%. Moreover, precise localization of a structural lesionelative to the functional area is indispensable to evaluatehe surgical risk and the possibility for complete resection,hich may be necessary to control seizures in many cases.

The International League Against Epilepsy recommendso perform an MRI in any patient with epilepsy, unless theres unequivocal evidence of idiopathic generalized or benignhildhood epilepsy. It also recommends MRI in patients whoevelop seizures in adulthood or when seizures are diffi-ult to control or have changed pattern. MRI is indicatedhen focal onset is suspected, even with previous nega-

ive studies. Periodical follow-up is required in lesions thatould potentially grow or bleed, irrespective of the clini-al manifestations. Some lesions can go undetected duringhe process of brain maturation, therefore once myelina-ion is completed (24---30 months) the MRI study should beepeated.

Brain injuries should be ruled out after an initialeizure. The clinical manifestations and the patient’s ageill determine the choice of imaging technique to besed. The primary cause of seizures in the neonate isypoxia/ischemia; trauma and tumors in adults; and infarc-ions in the elderly. Although MRI is the technique of choicen patients with epilepsy, computed tomography (CT) hasn important role in emergency situations given its highervailability, ease of retrieval, and its high sensitivity toetect acute hemorrhage, bone lesions or expanding lesions.onversely, febrile seizures do not require imaging eval-ation that should be reserved for patients younger thanne year, when there are other neurologic abnormalities,linical or electroencephalographic (EEG) suspicion of focalpilepsy.

Surgical treatment should always be considered inatients with refractory focal seizures --- defined as seizureshat cannot be satisfactorily controlled with two antiepileticrugs (AEDs)---in order to control seizures and/or improveheir quality of life. In these cases, MRI findings are par-icularly important because when they are consistent withhe clinical and EEG findings, no further examinations will
e required. In refractory seizures, MRI can detect 80% ofhe causative lesions in the temporal lobe and 60% in therontal lobe. The postoperative outcome is clearly better
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hen the structural lesion is detected.1 However, struc-ural MRI has limitations secondary to its inability to detectome lesions and the potential poor correlation with clini-al/EEG findings. In case of negative MRI, functional studiesre recommended (photon emission tomography [PET] orctal single-photon emission tomography [SPECT]), usuallyn combination with MRI to increase effectiveness. MR spec-roscopy has proved useful in temporal lobe epilepsy (TLE),nd although other advanced techniques such as diffu-ion and perfusion MRI seem promising, they need furtheralidation. Lastly, individualized preoperative evaluationf the patient with epilepsy should be performed at aultidisciplinary Epilepsy Unit (neurologist, neurosurgeon,

euroradiologist, and neuropsychologist) where the mostffective combination of diagnostic techniques for each par-icular case will be established.

agnetic resonance protocol

RI has changed the diagnosis of epilepsy not only radically,ut also gradually, as the technological developments, inoth hardware and software, have allowed for higher qual-ty images.2 In epilepsy, the highest quality imaging is alwaysecommended. Many studies have shown that field magnets1.5 T are absolutely contraindicated and that standard MRmaging is inadequate as it reduces significantly the diagnos-ic accuracy.3,4

The main objective of any structural study in patientsith epilepsy is to achieve maximum tissue contrastetween gray (GM) and white matter (WM) with high spatialesolution, in both the section (acquisition matrix) andhe section thickness, which should range between 0.5nd 1 mm for 3D studies and 2 and 4 mm for 2D studies.t present, 1.5 T systems are the most commonly usednd if used with appropriate protocols they would solveost cases, except for some subtle malformations. 3 Tagnets are being increasingly used in epilepsy5 and theyill probably replace 1.5 T systems as they become morevailable in reference centers. Nonetheless, 1.5 T magnetsill continue to be used in a more standard setting butith special protocols that will allow for the detection of

esions in a more efficient manner and the possibility ofonsultation with epilepsy centers without having to repeathe MRI study, which would increase the cost of the processnd unnecessary sedation in children.

T1 sequences should be obtained in 3D mode, withsotropic voxel of 1 mm and including the whole brain. Usu-lly, inversion-recovery prepared gradient echo (GE) pulseequences are used to increase GM/WM contrast (unlike spincho [SE] sequences). They allow reconstruction in any planeithout losing image quality, permitting, if necessary, vol-me rendering or curved reformations.

In the study of epilepsy, the hippocampus should alwayse evaluated in detail even when electroclinical data are notuggestive of temporal lobe epilepsy. Coronal sections per-endicular to the hippocampus should be obtained becausehey provide more information as well as high-resolution

hat for a field of view (FOV) of 240 mm the matrix shoulde ≥512. Three-dimensional sequences cannot be used tohis end because the acquisition time required with the

Structural magnetic resonance imaging in epilepsy 11

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Figure 1 Probable focal cortical dysplasia (not confirmed). T2is more clearly visible on the FLAIR sequence.

current techniques would be too long. Instead, 2-D fast-SE sequences (also called turbo-SE, depending on the MRsystem) should be used, with a 3 mm section thickness.FLAIR sequences in the same planes should also be usedto detect contrast changes rather than to detect morpho-logical or internal structural changes in the hippocampus.Section resolution could be lower, with matrices of 256 anda section thickness of 3---4 mm. FLAIR sequences are moresensitive for the detection of small signal changes than T2sequences, especially in areas adjacent to the cerebrospinalfluid (Fig. 1).6

Since fast-SE technique has low sensitivity to mag-netic susceptibility, lesions containing calcification orhemosiderin such as small cavernomas7 may not be detected(Fig. 2). For this reason, the study should be completed with4---5 mm section axial T2* sequences, obtained with eitherstandard GE technique or echo-planar imaging (EPI), whichare faster and do not require high-resolution matrices.

Moreover, even if a temporal origin is highly suspected,a whole-brain study using axial FLAIR sequences (alterna-tively T2) should be performed to rule out small lesions thatdirectly cause the seizure, or lesions associated with an hip-pocampal abnormality (dual pathology), with similar findingson the coronal images. Imaging with multichannel coils isalways recommended because they increase the signal andshorten imaging times, usually never less than 40 min. Inshort, a basic epilepsy protocol includes 3D-T1, coronal T2and FLAIR sequences and axial FLAIR and T2* sequences(Table) (Fig. 3).

Postcontrast sequences are not indicated in a basicepilepsy protocol, unless the clinical or imaging findingsmake it necessary the evaluation of a specific lesion, par-
ticularly in case of suspected tumor.
3 T magnets have the advantage of increasing the signal-to-noise ratio in an almost linear relationship to the field andimproving image contrast in T2. This results in an increase

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nd FLAIR (B) sequences. The small juxtacortical lesion (arrows)

n resolution and contrast, using acquisition times similaro those used in a standard protocol. A field of 3 T alsollows for high-resolution matrices (of up to 1024) in T2equences, a decrease of section thickness to 1---2 mm in 2Dequences8 and to 0.7 mm in 3D sequences (Fig. 4). In addi-ion, the increased signal allows the acquisition of 3D-FLAIRequences that offer enhanced detection and delimitation ofmall lesions. The use of 3 T systems for the study of patientsith refractory epilepsy is limited due to the scarce avail-bility. Although the use of high-field MR systems is reservedor individual patients in Epilepsy Units, they should be usedn any patient with refractory epilepsy with negative or non-onclusive findings following appropriate protocols using a.5 T MR system.

esial temporal sclerosis

ippocampal sclerosis is the most common feature of TLE,nd the most common cause of refractory epilepsy. His-ologically, there is neuronal loss, mossy fiber synapticeorganization and astrogliosis. The abnormalities are moreevere in certain areas of the hippocampus. In this respect,he Sommer sector (CA1 field) is the most vulnerable ands always impaired in MTS, with the most intense neuronaloss. The Bratz sector (CA3 and CA4 fields) is less frequentlynvolved. The CA2 field or Spielmeyer sector is the mostesistant. This means that there is selective vulnerability,ot only in the brain but also within the hippocampus, andhat seizures play an important role in the development ofTS.

Although the cause of MTS is not clearly established, in
act, there is probably more than one cause, it seems toe accepted that some type of insult during developmentamages the hippocampus in predisposed individuals, whoevelop MTS after the seizures begin. Complicated febrile

12 J. Álvarez-Linera Prado

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Figure 2 T2-FSE (A) and T2-EPI (B) sequences. The small left

eizures and status epilepticus are associated with MTS in upo 80% of cases. Patients with status epilepticus have shown
ostictal abnormalities in the hippocampus and amygdalaFig. 5).9 Postictal abnormalities of the hippocampus maye unilateral with postcontrast enhancement in the Som-er sector, reduction in the apparent diffusion coefficient,
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igure 3 Epilepsy protocol. Coronal 3D reformatted T1 weighted

nd axial T2-EPI (E) sequences.

etal cavernoma is visible on T2-EPI but undetected on T2-FSE.

nd, on follow-up imaging, may also show volume loss andildly increased signal intensity on T2 sequences (Fig. 6).

10
any of these cases develop subsequent TLE. Althoughhe presence of a previous insult in the hippocampus hasot been clearly established, it seems probable that abnor-al development of the hippocampus play an important
image (A), coronal T2 (B) and FLAIR images (C), axial FLAIR (D)


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Figure 4 High-resolution T2 (A) 3D-T1 (B) images obtained wdetailed assessment of the cortex and gray---white matter junct

role since, although MTS may develop in adulthood, mostpatients report a precipitating event during childhood.

The most common MRI finding in MTS is hippocampalatrophy (90---95%) followed by abnormal signal, especiallyhypersignal on T2/FLAIR sequences (80---85%), and loss ofinternal structure (60---95%)11,12 (Fig. 7). However, techni-cal factors have played a role in the frequency of findingsbecause as sequences and especially MR magnets haveimproved, more subtle changes in signal and internal struc-ture without significant loss of hippocampal volume arebeing detected.13,14 This is typical of endfolium sclerosis,
a histological subtype of MTS where the lesions are limitedto the CA3 and CA4 fields. In this pattern, the only findingcould be the increased signal in the central region of thehippocampus on T2 or FLAIR sequences.15 In doubtful cases,
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Figure 5 Left frontal focal cortical dysplasia (A and B) (short

hippocampi that is not visible on the FLAIR sequence (C), but clearly

3 T magnet. High spatial and contrast resolution allow a more

he use of 3 T MR systems increases the sensitivity (Fig. 8).n addition, when the volume loss is not conspicuous, loss ofigitations in the head of the hippocampus may be indica-ive of focal atrophy. MRI-based volumetric measurementsf the hippocampus may be useful in the research field andn doubtful cases especially when bilateral MTS is suspected,here visual analysis is more limited.16

In addition to the hippocampus, other structures of theimbic system may be involved, leading to secondary find-ngs. Dilatation of the ipsilateral temporal horn is common,lthough it has no value as isolated finding because asym-
etries of this structure also occur in healthy subjects.ccasionally, the amygdala can demonstrate hyperintensity,robably reflecting similar abnormalities to those of the hip-ocampus. Loss of volume of other limbic structures such as
arrows) with status epilepticus and postictal edema in both visible on the diffusion-weighted sequence (D) (long arrow).


Postcritical study

6 month follow-up

Postcritical study

1 month follow-up

1 year follow-up

6 month follow-up

Figure 6 Progression to hippocampal sclerosis of postictal edema in right hippocampus. Progression of the disease on T2 sequences(A, B, C and D) that show increased hippocampal size on the left side with gradual atrophy and increased signal. Isotropic diffusionM he Sot F) (a

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R images show initial restricted diffusion with hypersignal in to an increased diffusion coefficient that results in hyposignal (

he entorhinal cortex, fornix or the ipsilateral mammillaryody is less common, but these findings are usually asso-iated with conspicuous hippocampal changes, and theiriagnostic value is limited. According to autopsy studies,he contralateral hippocampus frequently shows histologicalhanges, but MRI findings do not exceed 20%.

Dual pathology---that is, MTS in association with another
esion---has been described in up to 15% of cases.17 Dualathology is most commonly seen in patients with disor-ers of the cortical development disorders (DCD). However,
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igure 7 Left medial temporal sclerosis. T2 (A) and FLAIR (B) sequarrows).

mmer sector of right hippocampus (arrow) (E) that progressesrrow).

he frequency and nature of some anomalies associatedith MTS remains unclear. Up to 65% of patients with MTSad subtle signal abnormalities in the WM of the tempo-al lobe,18 visible as poorly defined high signal on FLAIRequences, sometimes with a blurred cortical---subcorticalunction (Fig. 9). Some histological studies suggest thatnly changes in myelination of the temporal lobe occur,19

hile others have described type I FCD.20 It remains unclearhether these changes play a role in the development ofTS or MTS is the consequence of these changes, as it alters

ences show reduced hippocampal volume and increased signal


Figure 8 Examples of medial temporal sclerosis. Left images: T2 FSE sequence obtained with a 1.5 T magnet shows little atrophyand diffuse signal changes in left hippocampus (A). These changes are more evident on the same sequence obtained with a 3 T

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system (B). Right images: example of isolated sclerosis of the en(D) sequences.

temporal lobe maturation. In any case, it is important todetect the structural abnormalities associated with MTS,because, regardless of the etiologic factors, the outcome forselective amygdalohippocampectomy is worse in patientswith dual pathology. Resection of both lesions is, when pos-sible, recommended.

Several subtypes of MTS21 have been described, whichare being increasingly identified as the quality of MRIstudies improves. The most common type is ‘‘unilateral

Figure 9 Dual pathology in left temporal lobe. Signs of medialtemporal sclerosis (atrophy of the head of the hippocampus withloss of digitations) and white matter hyperintensity in temporallobe, with blurred cortical margin.

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um (CA3 and CA4). Increased central signal on T2 (C) and FLAIR

iffuse hippocampal sclerosis’’, which shows the typical MRIndings. In ‘‘unilateral anterior sclerosis’’, only the head ofhe hippocampus is involved.22 This is a less common causef refractory epilepsy that tends to develop later in life thanhe unilateral diffuse type (Fig. 10). Seizures in ‘‘temporo-ccipital epilepsy with MTS’’ may arise exclusively fromhe occipital lobe, but usually they spread to the temporalr frontal lobe. Association of an occipital focus with MTSs regarded as secondary MTS that results from the spreadf epileptogenic activity to the temporal lobe.23 ‘‘Diffuseilateral sclerosis’’ (Fig. 10) has been described in 10% ofatients with refractory TLE.24 Seizures usually start earliern life and secondary generalization is more common than innilateral sclerosis. This suggests that specific lesions suchs meningoencephalitis or toxic-metabolic encephalopathyay be the cause of generalized seizures. Patients withiffuse bilateral sclerosis show more memory impairmentnd other cognitive abnormalities. In these patients, theurgical outcome is not as good and the cognitive seque-ae are usually more severe, because of the damage inhe contralateral hippocampus.

About 70% of patients with typical MTS are seizure-freefter surgery. Studies using several imaging modalities havehown that in case of typical MTS the presence of hip-ocampal atrophy is the major predictive factor of surgicaluccess,25,26 but optimal outcome is achieved when all theodalities provide similar findings. Surgery is not contraindi-

ated in contralateral atrophy, but the outcome is lessavorable and the neuropsychological sequelae more severe.mygdalohippocampectomy is not sufficient in temporo-ccipital epilepsy, as in dual pathology, where lobectomys recommended.

isorders of cortical development

CD are common in patients with epilepsy, particularly thosehose epilepsy develops in childhood. They result from


Figure 10 Examples of subtypes of medial temporal sclerosis. Unilateral anterior sclerosis (A, B) involving only the left head oft roph

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he hippocampus (arrow). Diffuse bilateral sclerosis (C) with at

isruption of the different stages of cortical developmenthat involves three consecutive but not isolated events:roliferation/apoptosis of neuroblasts within the germinalatrix, radial and tangential migration of neuroblasts from

he germinal matrix towards the periphery of the brain, lay-red organization of the cortex with formation of a networkf synaptic connections.27 Overall, about 15% of patientsith DCD have refractory seizures and surgery may help toontrol them in some cases.

The study protocol of DCD is in general more compre-ensive than that used in the rest of causative disordersf epilepsy. In addition to the standard 3D-T1 sequences,t present, 3D-T2 and 3D-FLAIR sequences can assess veryccurately small abnormalities in the cortical-subcorticalunction and in the adjacent WB.28 Three-dimensionalequences, the new phased array multichannel coils andigh-field magnets have significantly improved the efficacyf MRI in DCD.

In the neonate, 3D-T1 and T2 are the most usefulequences. FLAIR sequences, essential in adults, are ofimited value because the scarce myelination makes themess sensitive to detect small lesions. Continued myeli-ation causes a frank reversal of the WM hypointensityn T1 and hyperintensity on T2 sequences, produc-ng the adult intensity pattern at 24---30 months. Upo 6 months, T2 sequences are more reliable, and T1equences between 12 and 24 months. Between 6 and 12onths, reliability of MRI is particularly low, early imag-

ng is thus recommended, and if performed in infantslder than three months, it should be repeated after4 months.

Medical treatment should begin as soon as the DCD isiagnosed and MRI may help determine the optimal treat-ent, for example, vigabatrinin for tuberous sclerosis withest syndrome.29 When diffuse abnormalities are detected,

urgical treatment is not very effective---in contrast with
ocal lesions such as FCD---because incomplete resectionss the major predictor of poor outcome in the control ofeizures.30 Determining the type of disorder is of particu-ar help for prognosis and genetic counseling. The degree
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y and increased signal of both hippocampi.

f impairment usually correlates with the extent of thealformation; for instance, in band heterotopia the thick-

ess of the band correlates with the degree of psychomotormpairment and with treatment failure. In schizencephaly,left size and bilaterality determine the outcome. Some MRIndings can lead to the molecular defect diagnosis caus-

ng the DCD. In this respect, mutations of the LIS1 genere responsible for parieto-occipital pachygyria (frontalachygyria is probably secondary to mutations of the DCXene), and mutations of the FLM gene are responsibleor periventricular heterotopia, which determines geneticounseling.31

There are three groups of DCD according to thearkovich classification27 that are based on the stage ofortical development primarily involved. Group I (prolif-ration) includes microcephaly and hemimegalencephaly,ype II FCD, tuberous sclerosis, and tumors such asysembryoplastic neuroepithelial tumor (DNT) and gan-lioglioma/gangliocytoma. Group II (migration) includesissencephaly, cobblestone cortex and heterotopias. GroupII (organization) includes polymicrogyria, schizencephalynd type I FCD (Table 1).

The Barkovich classification, based on embryologic crite-ia, is the most commonly used. Although this classificationemains fully in force, some novelties are attracting increas-ng attention, especially in FCD, not only because FCD arehe most common disorders in patients with refractory focaleizures, but also because surgical treatment is proving use-ul in many cases.

ocal cortical dysplasia

CD encompass a spectrum of disorders ranging from mild toevere cortical abnormalities, sometimes in association withther lesions including MTS or tumors with low proliferative
otential such as DNT or neuroglial tumors. Detection as wells characterization of DCF is crucial because the surgicalreatment and prognosis change depending on the type ofesion.

Structural magnetic resonance imaging in epilepsy

Table 1 Classification for malformations of corticaldevelopment.

I. Malformations due to abnormal neuronal or glialproliferation or apoptosisA. Brain size anomalies (decreasedproliferation/increased apoptosis, or increasedproliferation/decreased apoptosis)

1. Microcephaly with thin or normal cortex2. Microlissencephaly (extreme microcephaly with

thick cortex)3. Microcephaly with extensive polymicrogyria4. Macrencephaly

B. Abnormal proliferation (abnormal cell types)1. Non neoplastic:

(a) Cortical hamartomas of tuberous sclerosis(b) Cortical dysplasia with balloon cells(c) Hemimegalencephaly

2. Neoplastic:(a) Dysembryoplastic neuroepithelial tumor(b) Ganglioglioma(c) Gangliocytoma

II. Malformations due to abnormal neuronal migrationA. Lissencephaly/band heterotopia spectrumB. Cobblestone complex/Congenital muscular dystrophysyndromesC. Heterotopia

(a) Subependymal (periventricular)(b) Subcortical (except band heterotopia)(c) Marginal glioneuronal

III. Malformations due to abnormal cortical organizationA. Polymicrogyria and schizencephaly

(a) Bilateral polymicrogyria(b) Schizencephaly(c) Polymicrogyria with other brain abnormalities(d) Polymicrogyria or schizencephaly as part of

multiple congenital anomaliesB. Cortical dysplasia without balloon cellsC. Microdysgenesis

IV. Malformations of cortical development, not otherwiseclassifiedA. Malformations secondary to congenital errors ofmetabolism

(a) Mitochondrial and pyruvate deficit metabolicdisorders

(b) Peroxisomal disordersB. Other unclassified malformations

(a) Sublobar dysplasia(b) Others

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Modified from Barkovich et al.27

Typical signs of FCD are abnormal gyral pattern, corticalthickening, indistinct junction between GM-WM and signalchanges of WM, usually without expansion effect. 1.5 T MRIsystems may not detect some FCD. In fact, one of the mainapplications of 3 T system is the diagnosis of FCD. One of
the most relevant studies conducted in 45 patients with his-tologically confirmed lesions revealed that 3 T MR systemsmay detect up to 40% more lesions compared to standard
ill

17

.5 T, motivating a change in clinical management in morehan 35% of cases32 (Fig. 11).

The most common histological findings of FCD areisorganized cortical architecture (dyslamination)92%), increased number of molecular layer neurons62%), increased neuron size (cytomegalia) (62%), dysplasticeurons and balloon cells (37%). Other findings are lessommon.33,34 Grading of FCD is based on the severity ofhe abnormalities: the mildest degree is the architecturalysplasia with dyslamination. A more severe degree ishe cytoarchitectural dysplasia with cytomegalic neurons.aylor’s dysplasia is considered the most severe abnor-ality, with dysplastic neurons with or without balloon

ells. Palmini35 proposes a classification of cortical dys-lasia based on these histological features: type I referso lesions with dyslamination (type Ia or architectural)r cytomegaly (type Ib or cytoarchitectural), and type IIthe Taylor-type) refers to the presence of dysmorphiceurons (type IIa) with balloon cells (IIb). Much of thenterest in differentiating these two histological typesrises from recent publications that suggest the pos-ibility of characterization using MRI and, particularly,he fact that their different clinicopathologic features36

re associated with varied surgical success.37 Both typesave characteristic imaging findings.38 Abnormalities inCD type I (Fig. 12) may extend to one or multiple lobesnd are frequently associated with volume loss of WM,ithout thickening or abnormal cortical pattern, andithout cortical signal changes. The subcortical WM usuallyxhibits a moderately increased signal on FLAIR sequencesnd, to a lesser degree, on T2 images, with blurring athe GM-WM junction. FCD type I are more difficult toetect than type II by MRI because of the minor corticalhanges and subtle WM abnormalities. The volume loss andssociation with perinatal events suggest the presence ofossible destructive lesions during the late stages of brainevelopment. FCD type I is most frequently encounteredn the temporal lobe and in association with MTS, and its thus considered as dual pathology. FCD type I is associ-ted with a clearly less favorable surgical outcome thanCD type II probably due to its higher extent and worseelimitation.

FCD type II (Fig. 11D) shows a more archetypal semi-logy with thickening and/or abnormal gyral pattern and,requently, cortical signal changes. There is poor correla-ion between cortical thickening on MRI and histologicalndings. This is probably due more to an abnormal sig-al from the juxtacortical WM---which simulates a thickenedortex particularly on FLAIR sequences (‘‘cortical pseudo-hickening’’)---rather than to true cortical thickening. Forhis reason, cortical thickening should be carefully evalu-ted with T1 and T2 sequences.39 WM abnormalities aresually more conspicuous, clearly visible on FLAIR sequencesn most cases, and represent one of the factors thatllow better detection by MRI. Abnormal WM signal usu-lly involves the entire thickness, from the cortex towardshe ventricle (transmantle dysplasia), like the vertex of ariangle located in the ventricle. This sign may be very

s almost exclusively found in FCD type II. Unlike type Iesions, type II lesions occur more commonly in the frontalobe.


Figure 11 Comparison between 1.5 T and 3 T systems in focal cortical dysplasia type I of the left frontal lobe (A and C), and typeII of the left frontal lobe (B and D). Signal changes are more conspicuous on sequences obtained with the 3 T system (C and D). Asfor dysplasia type II, the signal change extending towards the ventricle is more clearly visible.

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igure 12 Focal cortical dysplasia type I. Slight signal increasB) sequences, with blurred cortical margin, more conspicuous

Association of FCD with tumors such as DNT and gan-lioglioma should be suspected in the presence of cystsr nodules. Association with calcifications is more com-on in gangliogliomas. Contrast-enhanced T1 imaging is

ecommended when any of these findings is detected. Theresence of enhancement is very suggestive of tumors.

FCD are better visualized during the first month of life,hat is, when the peripheral regions of the cerebral hemi-pheres are not myelinated yet. There is more contrast ofhe dysplastic cortex and subcortical WM with the normalrain (with hypointensity on T1 and hyperintensity on T2equences, unlike adult brain). In adult brain the lesion isuch less conspicuous. Additionally, ischemic lesions in the

eonate are a common cause of epilepsy and are clearlyisible on diffusion-weighted images during acute phases.or this reason, an MRI epilepsy protocol with diffusionequences is recommended in neonates with seizures.

iths

row) in white matter of right temporal lobe on T2 (A) and FLAIRe FLAIR image.

onclusion

tructural MRI is an essential part of the diagnostic processf epilepsy and involves a specific protocol with high spa-ial and contrast resolution. Most lesions causing refractorypilepsy can be visualized on structural MRI and its detections crucial for subsequent diagnostic and therapeutic plan-ing and, in the event of a negative MR, one must alwaysonsider the possibility of increasing image quality. MTSnd DCD, especially FCD, are common causes of refractorypilepsy exhibiting a characteristic semiology. Understand-ng of the different manifestation on structural MR imagess thus very important, as well as the possible associations
n dual pathology of MTS or between FCD and neuroglialumors. Nonetheless, some lesions such as FCD type I mayave a negative or non-conclusive structural study or, onome occasions, incidental lesions unrelated to epilepsy may

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Structural magnetic resonance imaging in epilepsy

be discovered. Correlation with electro-clinical data is thusessential and, in non-conclusive cases, functional studies,such MRI coregistered PET or ictal SPECT, should also beconsidered. However, these examinations, as with invasiveelectrodes, must be assessed in dedicated epilepsy units,with a multidisciplinary approach.

Conflict of interest

The author declares not having any conflict of interest.

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