Focal Cortical Dysplasia Lesions Research Articles

Cortical feature analysis and machine learning improves detection of "MRI-negative" focal cortical dysplasia.

Focal cortical dysplasia (FCD) is the most common cause of pediatric epilepsy and the third most common lesion in adults with treatment-resistant epilepsy. Advances in MRI have revolutionized the diagnosis of FCD, resulting in higher success rates for resective epilepsy surgery. However, many patients with histologically confirmed FCD have normal presurgical MRI studies ('MRI-negative'), making presurgical diagnosis difficult. The purpose of this study was to test whether a novel MRI postprocessing method successfully detects histopathologically verified FCD in a sample of patients without visually appreciable lesions. We applied an automated quantitative morphometry approach which computed five surface-based MRI features and combined them in a machine learning model to classify lesional and nonlesional vertices. Accuracy was defined by classifying contiguous vertices as "lesional" when they fell within the surgical resection region. Our multivariate method correctly detected the lesion in 6 of 7 MRI-positive patients, which is comparable with the detection rates that have been reported in univariate vertex-based morphometry studies. More significantly, in patients that were MRI-negative, machine learning correctly identified 14 out of 24 FCD lesions (58%). This was achieved after separating abnormal thickness and thinness into distinct classifiers, as well as separating sulcal and gyral regions. Results demonstrate that MRI-negative images contain sufficient information to aid in the in vivo detection of visually elusive FCD lesions.

Surgery for focal cortical dysplasia in children using intraoperative mapping.

Children with malformation of cortical development represent a significant proportion of pediatric epilepsy surgery candidates. Here, we describe a single-center experience with pediatric patients who underwent surgery for intractable epilepsy due to focal cortical dysplasia (FCD). Clinical data of 78 patients under 18years of age with diagnosis of intractable epilepsy due to FCD who underwent surgery from January 1996 to January 2012 were reviewed comparing data of patients submitted to electrocorticography (ECoG) with those without ECoG. Patients' mean age at surgery was 8.52 ± 4.99years; mean age at epilepsy onset was 2.55 ± 3.01years. Almost 80% of the patients underwent ECoG register that was essential for delimitation of surgical resection in 66 out of 78 patients. ECoG was performed in all patients with extratemporal lesions, and the most common FCD found was type II. Seizure outcome was similar in groups with or without ECoG. Tailored resection of FCD lesions for intractable epilepsy can be safely performed in children with a good seizure outcome and low complication rate. Epilepsy surgery should be considered for all patients with FCD and refractory epilepsy.

Estimating blur at the brain gray-white matter boundary for FCD detection in MRI.

Focal cortical dysplasia (FCD) is a frequent cause of epilepsy and can be detected using brain magnetic resonance imaging (MRI). One important MRI feature of FCD lesions is the blurring of the gray-white matter boundary (GWB), previously modelled by the gradient strength. However, in the absence of additional FCD descriptors, current gradient-based methods may yield false positives. Moreover, they do not explicitly quantify the level of blur which prevents from using them directly in the process of automated FCD detection. To improve the detection of FCD lesions displaying blur, we develop a novel algorithm called iterating local searches on neighborhood (ILSN). The novelty is that it measures the width of the blurry region rather than the gradient strength. The performance of our method is compared with the gradient magnitude method using precision and recall measures. The experimental results, tested on MRI data of 8 real FCD patients, indicate that our method has higher ability to correctly identify the FCD blurring than the gradient method.

Automated detection of cortical dysplasia type II in MRI-negative epilepsy.

To detect automatically focal cortical dysplasia (FCD) type II in patients with extratemporal epilepsy initially diagnosed as MRI-negative on routine inspection of 1.5 and 3.0T scans. We implemented an automated classifier relying on surface-based features of FCD morphology and intensity, taking advantage of their covariance. The method was tested on 19 patients (15 with histologically confirmed FCD) scanned at 3.0T, and cross-validated using a leave-one-out strategy. We assessed specificity in 24 healthy controls and 11 disease controls with temporal lobe epilepsy. Cross-dataset classification performance was evaluated in 20 healthy controls and 14 patients with histologically verified FCD examined at 1.5T. Sensitivity was 74%, with 100% specificity (i.e., no lesions detected in healthy or disease controls). In 50% of cases, a single cluster colocalized with the FCD lesion, while in the remaining cases a median of 1 extralesional cluster was found. Applying the classifier (trained on 3.0T data) to the 1.5T dataset yielded comparable performance (sensitivity 71%, specificity 95%). In patients initially diagnosed as MRI-negative, our fully automated multivariate approach offered a substantial gain in sensitivity over standard radiologic assessment. The proposed method showed generalizability across cohorts, scanners, and field strengths. Machine learning may assist presurgical decision-making by facilitating hypothesis formulation about the epileptogenic zone. This study provides Class II evidence that automated machine learning of MRI patterns accurately identifies FCD among patients with extratemporal epilepsy initially diagnosed as MRI-negative.

Expression and Cellular Distribution of the Interleukin 2 Signaling System in Cortical Lesions From Patients With Focal Cortical Dysplasia

Focal cortical dysplasia (FCD) is a well-known cause of medically intractable epilepsy. To understand the potential role of the inflammatory cytokine interleukin 2 (IL-2) in the pathogenesis of FCD, we investigated the expression patterns of IL-2 and its receptors (IL-2Rs) in FCD and control samples that included epileptic neocortex from mesial temporal lobe epilepsy patients and nonepileptic normal cortex (CTX). Greater mRNA and protein levels of IL-2 and IL-2Rs were observed in FCD versus CTX samples. Moreover, the expression of IL-2 and IL-2Rs was significantly higher in FCD II than FCD I. In situ hybridization and immunohistochemistry results indicated that IL-2 and IL-2Rs were strongly expressed in hypertrophic neurons and neuronal microcolumns in FCD I and highly expressed in malformed cells in FCD II. In addition, the protein levels of Janus kinase 1, Janus kinase 3, phosphorylated signal transducer and activator of transcription 5, which are important downstream factors in the IL-2 signaling pathway, were increased in FCD lesions. Soluble IL-2R was decreased in FCD compared with that in CTX samples. These results suggest that upregulation of IL-2 and IL-2Rs combined with activation of IL-2-dependent signaling pathways may contribute to the pathogenesis of FCD.

3 TESLA MR imaging in adults with focal onset epilepsy

ObjectiveThe finding of cerebral epileptogenic lesions in magnetic resonance (MR) has demonstrated to be a relevant prognostic factor for potential surgical candidates. In a series of consecutive adults with focal onset epilepsy, we investigated the yield of 3T MR imaging for detecting epileptogenic cerebral lesions. Materials and methodsWe prospectively recruited 161 adult patients with a diagnosis of focal epilepsy, all of whom underwent standardized MR imaging study performed with a 3T magnet. ResultsLesion-related epilepsy was observed in 48% of patients, and 12% of cryptogenic patients showed subtle or non-specific lesions related to the epileptogenic source. The most common findings were focal cortical dysplasia and vascular lesions, followed by mesial temporal sclerosis, tumors, and scars from previous cerebral injuries. Patients older than 72 years were more likely to have vascular epilepsy. ConclusionsDiagnostic assessment using a standardized 3T MR imaging protocol for focal-onset epilepsy detects lesions in nearly half the patients. Our results indicate that elders with focal epilepsy should be searched for vascular lesions.

Seizure control after subtotal lesional resection

Reports on seizure outcomes following surgery for lesional epilepsy consistently cite extent of resection as a significant predictor of outcome. Unfortunately, gross-total resection is not technically feasible in all cases of medically refractory tumor-associated epilepsy. Here, the authors present the case of a 4-year-old girl whose epilepsy was medically controlled after 1-stage electrocorticography-guided subtotal resection (STR) of a large diffuse protoplasmic astrocytoma. They also review the modern literature on epilepsy associated with brain tumors. Outcomes are compared with those following surgical treatment of focal cortical dysplasia and vascular lesions. Gross-total lesional resection shows significant superiority across pathologies and anatomical regions. Despite a considerable number of STRs yielding seizure freedom, other favorable treatment factors have not been defined. Although gross-total lesional resection, if possible, is clearly superior, tailored surgery may still offer patients a significant opportunity for a good outcome. Treatment factors yielding successful seizure control following STR remain to be fully elucidated.

MR imaging features of epileptogenic focal cortical dysplasia and optimization of scanning protocols

Objective To analyze the MR imaging features of epileptogenic focal cortical dysplasia (FCD)and to optimize the scanning protocols by correlating MRI appearance with pathological findings.Methods MRI findings and the relative scanning protocols in 36 patients with surgically and pathologically proved 40 lesions of FCD were retrospectively analyzed. According to Palmini classification system,all 40 lesions were pathologically categorized as FCD type Ⅰ (including FCD Ⅰ A and FCD Ⅰ B) and FCD type Ⅱ (including FCD Ⅱ A and FCD ⅡB ). The distribution of cerebral or dual lesions accompanied hippocampal sclerosis were observed.Differences of the distribution of cerebral in FCD type Ⅰ and FCD type Ⅱ were compared by using Fisher exact probabilities. MR scans in all patients consisted of routine and optimized protocols.Axial FSE T2WI,axial SET1WI and axial FLAIR were recognized as routine scanning protocols,while adding oblique coronal FSE T2WI and FLAIR were recognized as optimization scanning protocols.Both routine and optimization scanning protocols were performed in all patients.The conspicuity of main findings of FCD on different imaging plane and sequences of each protocol were assessed.The detection of cerebral or dual lesion and the accompanied hippocampal sclerosis were compared between the routine protocol and the optimized protocol by using McNemar test.Results Forty lesions were found in 36 cases with FCD,29 had temporal lobe lesion (72.5％ ),9 had frontal lobe lesion(22.5％ ) and 2 had parietal lobe lesion (5.0％).According to Palmini classification system,29 lesions in 27 patients (72.5％ ) were FCD type Ⅰ,11 lesions in 10 patients (27.5％) were FCD type Ⅱ lesions.There were 25 temporal lobe lesions in FCD type Ⅰ,while 4 in FCD type Ⅱ.There were statistically significant differences between FCD type Ⅰ group and FCD type Ⅱ group in the distribution of cerebral (P =0.002 ).Fourteen cases were found to have hippocampal sclerosis simultaneously,with 13 cases found in FCD type Ⅰ patients and 1 case in type Ⅱ patients.The detection rate of temporal lobe lesion was 65.5 ％ (19/29) and 44.8 ％ ( 13/29 ) respectively on optimized protocol and routine protocol.There was statistically significant difference ( x2 =4.167,P =0.031 ).The detection rate of hippocampal sclerosis was 85.7％ (12/14) and 42.9％ (6/14) respectively on optimized protocol and routine protocol respectively.There was statistically significant difference ( x2 =4.167,P =0.031 ).The detection rate of frontal lobe lesion showed no statistically significant difference between optimized protocols and routine protocols (x2 =0.304,P =1.000 ).Conclusions FCD was frequently involved the temporal lobe,followed by the frontal lobe.FCD type Ⅰ lesion was frequently found in the temporal lobe,with a higher incidence of concomitant hippocampal sclerosis. The optimized whole temporal lobe scanning with imaging plane perpendicular to the hippocampus long axis was a highly desired scanning protocol specifically for FCD,which is helpful for the detection of the FCD lesions. Key words: Cerebral cortex; Nervous system abnormalities; Magnetic resonance imaging

Focal cortical dysplasia coexisting with diffuse astrocytoma in childhood: A case report and reappraisal of the glial component in archival FCD cases

We report a rare case of focal cortical dysplasia (FCD) concurring with diffuse astrocytoma and arachnoid cyst, and also re-evaluate the glial component in archival FCD cases for the differential diagnosis of diffuse gliomas. A 7-year-old boy with a 9-month history of psychomotor seizures disclosed a hyperintense area accompanied by a cystic lesion in the left temporal lobe on MRI. The surgical specimen displayed dyslamination of the cortices and ectopic neurons in the white matter, associated with dysmorphic neurons, indicating FCD type IIA. Additionally, the lesion showed diffuse proliferation and infiltration of glial cells, immunopositive for infiltrating glioma markers (nestin, doublecortin, MAP-2e) and p53, and MIB-1 index was 2.0%. These findings indicated coexisting diffuse astrocytoma. Coexistence of diffuse glioma with FCD is unusual, but we often notice increased population of small glial cells in FCD lesions. Re-evaluation of archival FCD cases with diverse markers revealed that reactive microglia significantly proliferate in the white matter lesions. Therefore, a careful pathological assessment has to be made to define a rare case of diffuse glioma occurring in FCD.

Clinicopathological features and surgical outcomes of intractable epilepsy due to focal cortical dysplasia

Objective To study the correlation with subtypes of focal cortical dysplasia(FCD) and surgical outcomes in patients with intractable epilepsy due to FCD.Method According to Palmini's FCD classification,the clinical,radioiogical and pathological features of 42 intractable epilepsy patients of FCD received surgical treatment were reviewed retrospectively.Results Among 42 epilepsy patients,the FCD lesions were located in 24 temporal lobes,14 frontal lobes,6 parietal lobes,3 occipital lobes,5 multilple lesions.The positive rate of preoperative MRI examination was 62%.The subtypes of FCD were identified as following:FCD type Ⅰ A in 9,FCD type Ⅰ B in 21,FCD type Ⅱ A in 5 and FCD type Ⅱ B in 7,respectively.FCD type Ⅰ B was the predominant pathological subtype and almost located in temporal lobe associated hippocampal sclerosis.The curative rate of FCD surgery in temporal lobe epilepsy group was 67% and that in extratemporal group was 43% (Engle Ⅰ a)during follow -up period (at leastⅠ year).Conclusions FCD is a common cause of intractable epilepsy.The different intrinsic neuropathological characteristics,particularly the potential epileptogenic feature,have significant correlations with clinical findings.Further study should be made between each category with its surgical outcome. Key words: Focal cortical dysplasia; Intractable epilepsy; Pathology; Surgical procedures,operative

Searching for the Lesion in “MRI-Normal” Neocortical Epilepsy—Plumb the Depths!

Small Focal Cortical Dysplasia Lesions Are Located at the Bottom of a Deep Sulcus. Besson P, Andermann F, Dubeau F, Bernasconi A. Brain 2008;131(Pt 12):3246–3255. Focal cortical dysplasia (FCD) is often characterized by minor structural changes that may go unrecognized by standard radiological analysis. Visual assessment of morphological characteristics of FCD and sulci harboring them is difficult due to the complexity of brain convolutions. Our purpose was to elucidate and quantify the spatial relationship between FCD lesions and brain sulci using automated sulcal extraction and morphometry. We studied 43 consecutive FCD patients using high-resolution MRI. Lesions were classified into small and large using qualitative (detection on initial clinical assessment of conventional MRI) and quantitative (volume) criteria. Sulci were identified and labeled automatically using an algorithm based on a congregation of neural networks. Segmented FCD lesions and sulci were then simultaneously visualized in 3D. We measured mean and maximum depth of sulci related to each FCD and of the corresponding sulci in 21 healthy controls. In addition, we calculated sulcal depth within the FCD neighborhood. Twenty-one (21/43 = 49%) patients had small FCD lesions (volume range: 128–3093 mm ( 3 )). Among them, 17 (81%) had been overlooked during initial radiological evaluation and were subsequently identified using image processing. Eighteen (18/21 = 86%) small FCD lesions were located at the bottom of a sulcus. Two others were related to the walls of two sulci and one was located at the crown of a gyrus. Mean and maximum depth of sulci related to the FCD was higher than that of the corresponding sulci in controls ( p < 0.008). Sulcal depth within lesional neighborhood had larger mean depth than that of the entire sulcus ( p < 0.0002). Evidence that small FCD lesions are preferentially located at the bottom of an abnormally deep sulcus may be used to direct the search for developmental abnormalities, particularly in patients in whom large-scale MRI features are only mildly abnormal or absent.

Focal Cortical Dysplasia (FCD) lesion analysis with complex diffusion approach

Identification of Focal Cortical Dysplasia (FCD) can be difficult due to the subtle MRI changes. Though sequences like FLAIR (fluid attenuated inversion recovery) can detect a large majority of these lesions, there are smaller lesions without signal changes that can easily go unnoticed by the naked eye. The aim of this study is to improve the visibility of focal cortical dysplasia lesions in the T1 weighted brain MRI images. In the proposed method, we used a complex diffusion based approach for calculating the FCD affected areas. Based on the diffused image and thickness map, a complex map is created. From this complex map; FCD areas can be easily identified. MRI brains of 48 subjects selected by neuroradiologists were given to computer scientists who developed the complex map for identifying the cortical dysplasia. The scientists were blinded to the MRI interpretation result of the neuroradiologist. The FCD could be identified in all the patients in whom surgery was done, however three patients had false positive lesions. More lesions were identified in patients in whom surgery was not performed and lesions were seen in few of the controls. These were considered as false positive. This computer aided detection technique using complex diffusion approach can help detect focal cortical dysplasia in patients with epilepsy.

Small focal cortical dysplasia lesions are located at the bottom of a deep sulcus

Focal cortical dysplasia (FCD) is often characterized by minor structural changes that may go unrecognized by standard radiological analysis. Visual assessment of morphological characteristics of FCD and sulci harbouring them is difficult due to the complexity of brain convolutions. Our purpose was to elucidate and quantify the spatial relationship between FCD lesions and brain sulci using automated sulcal extraction and morphometry. We studied 43 consecutive FCD patients using high-resolution MRI. Lesions were classified into small and large using qualitative (detection on initial clinical assessment of conventional MRI) and quantitative (volume) criteria. Sulci were identified and labelled automatically using an algorithm based on a congregation of neural networks. Segmented FCD lesions and sulci were then simultaneously visualized in 3D. We measured mean and maximum depth of sulci related to each FCD and of the corresponding sulci in 21 healthy controls. In addition, we calculated sulcal depth within the FCD neighbourhood. Twenty-one (21/43 = 49%) patients had small FCD lesions (volume range: 128-3093 mm(3)). Among them, 17 (81%) had been overlooked during initial radiological evaluation and were subsequently identified using image processing. Eighteen (18/21 = 86%) small FCD lesions were located at the bottom of a sulcus. Two others were related to the walls of two sulci and one was located at the crown of a gyrus. Mean and maximum depth of sulci related to the FCD was higher than that of the corresponding sulci in controls (P < 0.008). Sulcal depth within lesional neighbourhood had larger mean depth than that of the entire sulcus (P < 0.0002). Evidence that small FCD lesions are preferentially located at the bottom of an abnormally deep sulcus may be used to direct the search for developmental abnormalities, particularly in patients in whom large-scale MRI features are only mildly abnormal or absent.

Texte de la conférence de consensus des 3 et 4 mars 2004 organisée par l’Anaes : « prise en charge des épilepsies partielles pharmacorésistantes » (chapitre consacré à la chirurgie – question 3)

Recent ILAE classification defined focal cortical dysplasia (FCD) patients with accompanying epileptic lesions as a separate group. We investigated data of patients with sole FCD lesions regarding long-term seizure outcome and different characteristics of FCD type 1 and type 2 patients.Eighty children and adult patients underwent surgery for FCD were included to the analysis of factors differentiating FCD type 1 and type 2 groups and their effect on long-term outcome.FCD type 2 patients had earlier epilepsy onset (8.1 vs. 6.1 years. p = 0.019) and underwent surgery younger than type 1 (18.2 vs. 23.7 years. p = 0.034). FCD type 2 patients were more prominently MR positive (77.8% vs. 53.8%. p = 0.029), which increased within FCD type 2 group as patients become younger (p = 0.028). FCD Type 1 lesions showed mostly multilobar extension and FCD type 2 mostly located in frontal lobe. Seizure freedom was achieved in 65.4% of FCD type 1 patients and 70.4% of FCD type 2 patients. Seven patients had permanent de novo neurological deficits. Mean follow-up time was 5.5 years (Range: 1–11 years).Surgical intervention in carefully selected patients may facilitate favorable seizure outcome leading to better quality of life. FCD type 1 and type 2 groups present with evident differences, which may promote medical and surgical management of these pathologies.

Focal cortical dysplasia with calcification: a case report

Focal cortical dysplasia (FCD) with calcification is rare. We presented a 13-year-old epileptic patient with FCD and calcification in the left frontal lobe. At age 24, the FCD lesion and the surrounding epileptogenic cortex and underlying subcortex were removed after chronic subdural electrode recording. Histological examination showed that the calcified lesion was not independent of the FCD lesion but located in the subcortical area of the FCD lesion. A neoplastic nature was ruled out for the lesion. The pathophysiological mechanism involved in the coexistence of FCD and calcification is discussed.

Pathophysiologic characteristics of balloon cells in cortical dysplasia

Balloon cells are histopathological hallmarks of cortical malformations, i.e., focal cortical dysplasia (FCD) of the Taylor type or the cortical tubers of tuberous sclerosis, and they are believed to be the epileptogenic substrate and cause therapeutic drug resistant epilepsy in man. This study was carried out to investigate the developmental histogenesis and epileptogenesis of balloon cells in FCD. We used an immunohistochemical approach to examine the expressions of primitive neuroepithelial cell antigens (CD34, nestin, and vimentin), ionotrophic glutamate receptor subunits (NR1, NR2A/B, GluR1, GluR2, GluR3, GluR4, and GluR5/6/7), and P-glycoprotein in balloon cells from FCD and normal cerebral cortex epileptogenic lesions. Balloon cells presented in clusters or as scattered cells throughout FCD lesions involving the gray and white matter. We found the balloon cells to be classifiable into three subtypes based on glial fibrillary acidic protein (GFAP) and neurofilament protein (NF-L) immunohistochemistry, i.e., as neuronal, astrocytic, and uncommitted. Immunopositivity for nestin, CD34, and vimentin in balloon cells of FCD suggests that they may be derived from the abnormal development and differentiation of neural stem cells. Moreover, it appears that epileptogenesis in cortical dysplasia is partly caused by the upregulations of some glutamate receptor subunit proteins (NR1, NR2A/B, GluR1, and GluR3) in balloon cells and dysplastic neurons. We speculate that the presence of the drug resistance protein P-glycoprotein in balloon cells might explain medically refractory epilepsy in FCD.

Expression of CD34 as a novel marker for glioneuronal lesions associated with chronic intractable epilepsy

The spectrum of glioneuronal lesions underlying intractable epilepsies includes malformative pathologies like focal cortical dysplasia (FCD); and neoplastic lesions like gangliogliomas (GG) and dysembryoplastic neuroepithelial tumours (DNT). These may occur either singly or as dual lesions, having simultaneous presence of both elements. Currently, the relationship between the malformative and neoplastic glioneuronal lesions is poorly understood. Recently, CD34, a stem cell marker transiently expressed during early neurulation, has been identified in these tumours. This study was undertaken to (i) evaluate the role of CD34 as a diagnostic marker for glioneuronal lesions of epilepsy, namely, GG, DNT and FCD, and (ii) attempt to define the relationship among these lesions, using CD34 as a marker. Tissues resected from 47 patients with intractable epilepsy due to glioneuronal lesions (GG, FCD, DNT) were studied. These were evaluated for CD34 expression, using immunohistochemistry. Dysplastic or atypically differentiated neural precursors which could not be identified on routine haematoxylin and eosin (H&E) staining were highlighted by CD34 immunostaining. The pattern of immunostaining was diffuse in GGs, unlike FCDs, wherein cells were present singly or in small clusters. However, cases of DNT and control tissue were largely CD34-immunonegative. Based on these findings, we propose a possible common origin of GG and FCD, from a bipotent precursor that undergoes abnormal glioneuronal development, while DNTs possibly have a different origin. The CD34-immunoreactive cells represent dysplastic or undifferentiated neural precursors, which may signify a valuable marker for the diagnostic evaluation of neoplastic and/or malformative pathologies in patients with intractable epilepsy.

Segmentation of focal cortical dysplasia lesions on MRI using level set evolution

Focal cortical dysplasia (FCD) is the most frequent malformation of cortical development in patients with medically intractable epilepsy. On MRI, FCD lesions are not easily differentiable from the normal cortex and defining their spatial extent is challenging. In this paper, we introduce a method to segment FCD lesions on T1-weighted MRI. It relies on two successive three-dimensional deformable models, whose evolutions are based on the level set framework. The first deformable model is driven by probability maps obtained from three MRI features: cortical thickness, relative intensity and gradient. These features correspond to the visual characteristics of FCD and allow discriminating lesions and normal tissues. In a second stage, the previous result is expanded towards the underlying and overlying cortical boundaries, throughout the whole cortical section. The method was quantitatively evaluated by comparison with manually traced labels in 18 patients with FCD. The automated segmentations achieved a strong agreement with the manuals labels, demonstrating the applicability of the method to assist the delineation of FCD lesions on MRI. This new approach may become a useful tool for the presurgical evaluation of patients with intractable epilepsy related to cortical dysplasia.

Neuroimaging of Focal Cortical Dysplasia

Focal cortical dysplasia (FCD) is a common cause of pharmacoresistant epilepsy that is amenable to surgical resective treatment. The identification of structural FCD by magnetic resonance imaging (MRI) can contribute to the detection of the epileptogenic zone and improve the outcome of epilepsy surgery. MR epilepsy protocols that include specific T1 and T2 weighted, and fluid-attenuated inversion recovery (FLAIR) sequences give complementary information about the characteristic imaging features of FCD; focal cortical thickening, blurring of the gray-white junction, high FLAIR signal, and gyral anatomical abnormalities. Novel imaging techniques such as magnetic resonance spectroscopy (MRS), magnetization transfer imaging (MTI), and diffusion tensor imaging (DTI) can improve the sensitivity of MR to localize the anatomical lesion. Functional/metabolic techniques such as positron emission tomography (PET), ictal subtraction single photon emission computed tomography (SPECT), functional MRI (fMRI), and magnetic source imaging (MSI) have the potential to visualize the metabolic, vascular, and epileptogenic properties of the FCD lesion, respectively. Identification of eloquent areas of cortex, to assist in the surgical resection plan, can be obtained non-invasively through the use of fMRI and MSI. Although a significant number of FCD lesions remain unidentified using current neuroimaging techniques, future advances should result in the identification of an increasing number of these cortical malformations.

In Vivo Profiling of Focal Cortical Dysplasia on High‐resolution MRI with Computational Models

On MRI, focal cortical dysplasia (FCD) is characterized by a combination of increased cortical thickness, hyperintense signal within the dysplastic lesion, and blurred transition between gray and white matter (GM-WM). The visual identification of these abnormal characteristics may be difficult, and it is unclear to what degree these features occur among different FCD lesions. Our purpose was to investigate the pattern of occurrence of abnormal MRI characteristics in FCD by using a set of computational models and to generate quantitative lesion profiling. A set of voxel-wise operators was applied to high-resolution 3D T1-weighted MRI in 23 patients with histologically proven FCD and 39 healthy controls, creating maps of GM thickness, maps of relative intensity highlighting areas with hyperintense signal, and maps of gradient magnitude modeling the GM-WM transition. All FCD lesions were segmented manually on the T1-weighted MRI. FCD volumes ranged from 734 mm3 to 80,726 mm3 (mean, 8,629 mm3 +/- 16,238). The manually segmented FCD lesions were used to estimate features in the lesional area and to determine possible local variations of each feature by means of a histogram. In 78% of the patients, FCD lesions were characterized by simultaneous GM thickening, hyperintense signal, and blurring of the GM-WM transition. Moreover, in all patients, the FCD lesion had at least two of these three characteristics. The three features occurred regardless of the lesion volume, and they characterized not only large FCD lesions, but also subtle ones that had been overlooked by conventional radiologic inspection before surgery.