Deep venous communication in vein of Galen malformations: incidence, Imaging, and Implications for treatment.

BACKGROUND: Failure to appreciate deep venous drainage pathways is a major cause of severe complications in the endovascular treatment of vein of Galen aneurysmal malformations (VOGMs). OBJECTIVE: To report deep venous drainage patterns in patients with VOGM, emphasizing the internal cerebral veins, and to describe the challenges in evaluating these. METHODS: Patients with VOGM presenting to our institute between 2000 and 2018 were retrospectively analyzed. Patients with complete and good quality imaging datasets were included in the study. Three neuroradiologists with expertise in the subject independently analyzed the deep venous drainage patterns on multi-sequence MRI and digital subtraction angiography. Follow-up imaging studies were analyzed for alterations in deep venous drainage patterns that occurred following endovascular treatment. Descriptive statistics were used to report findings. RESULTS: Twenty-three patients had optimal quality MRI imaging and 25 had optimal quality DSA imaging available. In 14/23 (61%) patients, internal cerebral vein (ICV) communication could be reliably identified on MRI and in 8/25 (32%) patients on DSA. Deep venous communication with the VOGM was demonstrated in 8/26 (30.8%) patients. One (3.8%) patient demonstrated ICV communication with the VOGM only on postoperative imaging, while in 2 (8%) patients the ICV drainage route changed from VOGM to alternative pathways after the procedure. Other variant pathways included lateral mesencephalic vein, superior or inferior sagittal sinus, anterior mesencephalic vein, tentorial sinus, deep Sylvian vein, and superior vermian vein. CONCLUSION: ICV communication with the VOGM is not uncommon and requires dedicated preprocedural imaging to identify it. However, there are significant challenges in assessing this communication in the presence of high-flow fistulae, vessel tortuosity and size, and contrast limitations in this population.

Pediatric Brain Tumor Genetics: What Radiologists Need to Know.

Brain tumors are the most common solid tumors in the pediatric population. Pediatric neuro-oncology has changed tremendously during the past decade owing to ongoing genomic advances. The diagnosis, prognosis, and treatment of pediatric brain tumors are now highly reliant on the genetic profile and histopathologic features of the tumor rather than the histopathologic features alone, which previously were the reference standard. The clinical information expected to be gleaned from radiologic interpretations also has evolved. Imaging is now expected to not only lead to a relevant short differential diagnosis but in certain instances also aid in predicting the specific tumor and subtype and possibly the prognosis. These processes fall under the umbrella of radiogenomics. Therefore, to continue to actively participate in patient care and/or radiogenomic research, it is important that radiologists have a basic understanding of the molecular mechanisms of common pediatric central nervous system tumors. The genetic features of pediatric low-grade gliomas, high-grade gliomas, medulloblastomas, and ependymomas are reviewed; differences between pediatric and adult gliomas are highlighted; and the critical oncogenic pathways of each tumor group are described. The role of the mitogen-activated protein kinase pathway in pediatric low-grade gliomas and of histone mutations as epigenetic regulators in pediatric high-grade gliomas is emphasized. In addition, the oncogenic drivers responsible for medulloblastoma, the classification of ependymomas, and the associated imaging correlations and clinical implications are discussed. ©RSNA, 2018.

Differential patterns of metastatic dissemination across medulloblastoma subgroups.

OBJECTIVE Metastatic dissemination is a major treatment challenge and cause of death in patients with medulloblastoma. However, the influence of molecular biology on the pattern of metastatic dissemination at diagnosis is not known. In this study, the authors sought to define the location, pattern, and imaging characteristics of medulloblastoma metastases across subgroups at diagnosis. METHODS A consecutive cohort of patients with metastatic medulloblastoma at The Hospital for Sick Children and the University Hospital Motol, who underwent up-front MRI of the craniospinal axis, was assembled and allocated to subgroups using NanoString limited gene-expression profiling. Radiological characteristics (including location, morphology, size, diffusion restriction, and contrast enhancement) were discerned through a retrospective review. RESULTS Forty metastatic medulloblastomas were identified with up-front neuroimaging of the craniospinal axis: 5 sonic hedgehog (SHH), 16 Group 3, and 19 Group 4 metastases. Significant subgroup-specific differences were observed, particularly with respect to tumor location, size, and morphology. Group 3 metastases were most frequently laminar compared with a more nodular pattern in Group 4 (14 of 16 in Group 3 vs 8 of 19 in Group 4; p = 0.0004). Laminar metastases were not observed in patients with SHH medulloblastoma. Suprasellar metastases are highly specific to Group 4 (p = 0.016). Two of the 5 SHH cases had multifocal lesions in the cerebellum, raising the possibility that these were in fact synchronous primary tumors and not true metastases. A minority of patients with Group 4 metastases harbored metastatic deposits that did not enhance on MRI after contrast administration, often in patients whose primary tumor did not enhance. CONCLUSIONS The location, morphology, and imaging characteristics of metastatic medulloblastoma differ across molecular subgroups, with implications for diagnosis and management. This suggests that the biology of leptomeningeal dissemination differs among medulloblastoma subgroups.

Cerebral hemispheric low-grade glial tumors in children: preoperative anatomic assessment with MRI and DTI.

PURPOSE: The aims of this study are to analyze how the nature and the behavior of low-grade glial tumors (LGGT) in children may correlate with the anatomy of the cerebral hemispheres and to evaluate the consequent impact of diffusion tensor imaging (DTI) techniques in the presurgical assessment. METHODS: This is a combined review of a series of 155 cases of LGGT and of the recent literature on the subject. RESULTS: The cases retrieved from our data bank were divided in central hemispheric tumors (basal ganglia and thalami) (36 cases), glioneuronal cortical-based tumors (49 cases), and glial tumors of the cerebral mantle (70 cases). A close correlation was found in the thalamus between the primary location of the tumor (juxta-ventricular, inferior, lateral, bilateral) and its extension (ventricular lumen, midbrain and mesial temporal, globus pallidus, respectively) which may relate to the connectivity. Among the glioneuronal tumors, most gangliogliomas were located in the temporal lobe and especially in the mesial temporal structures. In addition, the morphologic feature of the ganglioglioma was different there from the neocortical areas. As a complementary approach, DTI data may assist in evaluating the structure and the extension of the LGGT, in addition to planning the surgical strategy. CONCLUSIONS: In the cerebral hemispheres like in the rest of the central nervous system, there is some degree of correlation between the anatomy and the nature, appearance, and behavior of the LGGT in children.

Corpus callosum abnormalities: neuroradiological and clinical correlations.

AIM: To study neuroradiological features in pediatric patients with corpus callosum abnormalities, using new functional subtyping for the corpus callosum, and to correlate the features with the clinical presentation. METHOD: We performed a retrospective review of 125 patients with radiologically identified abnormalities of the corpus callosum seen between 1999 and 2012. The study reviewed clinical features, genetic etiology, and chromosomal microarray (CMA) results. We used a new functional classification for callosal abnormalities based on embryological and anatomical correlations with four classes: complete agenesis, anterior agenesis (rostrum, genu, body), posterior agenesis (isthmus, splenium), and complete hypoplasia (thinning). We also studied the presence of extracallosal abnormalities. RESULTS: The new functional callosal subtyping did not reveal significant differences between the various subtypes in association with neurological outcome; however, the presence of cardiac disease was found more frequently in the group with complete agenesis. Thirty-seven per cent (46/125) had identifiable causes: of these, 48% (22/46) had a monogenic disorder, 30% (14/46) had a pathogenic chromosomal copy-number variant detected by CMA or karyotype, and 22% (10/46) had a recognizable clinical syndrome for which no confirmatory genetic test was available (namely Aicardi syndrome/septo-optic dysplasia and Goldenhar syndrome). The diagnostic yield for a significant CMA change was 19%. The presence of Probst bundles was found to be associated with a better neurodevelopmental outcome. INTERPRETATION: The functional classification system alone 'without clinical data' cannot predict the functional outcome. The presence of extracallosal brain abnormalities and an underlying genetic diagnosis predicted a worse neurodevelopmental outcome. This study highlights the importance of CMA testing and cardiac evaluation as part of a routine screen.

Posterior fossa tumors in children: developmental anatomy and diagnostic imaging.

INTRODUCTION: Modern understanding of the relation between the mutated cancer stem cell and its site of origin and of its interaction with the tissue environment is enhancing the importance of developmental anatomy in the diagnostic assessment of posterior fossa tumors in children. The aim of this review is to show how MR imaging can improve on the exact identification of the tumors in the brainstem and in the vicinity of the fourth ventricle in children, using both structural imaging data and a precise topographical assessment guided by the developmental anatomy. RESULTS: The development of the hindbrain results from complex processes of brainstem segmentation, ventro-dorsal patterning, multiple germinative zones, and diverse migration pathways of the neural progenitors. Depending on their origin in the brainstem, gliomas may be infiltrative or not, as well as overwhelmingly malignant (pons), or mostly benign (cervicomedullary, medullo-pontine tegmental, gliomas of the cerebellar peduncles). In the vicinity of the fourth ventricles, the prognosis of the medulloblastomas (MB) correlates the molecular subtyping as well as the site of origin: WNT MB develop from the Wnt-expressing lower rhombic lip and have a good prognosis; SHH MB develop from the Shh-modulated cerebellar cortex with an intermediate prognosis (dependent on age); recurrences are local mostly. The poor prognosis group 3 MB is radiologically heterogeneous: some tumors present classic features but are juxtaventricular (rather than intraventricular); others have highly malignant features with a small principal tumor and an early dissemination. Group 4 MB has classic features, but characteristically usually does not enhance; dissemination is common. Although there is as yet no clear molecular subgrouping of the ependymomas, their sites of origin and their development can be clearly categorized, as most develop in an exophytic way from the ventricular surface of the medulla in clearly specific locations: the obex region with expansion in the cistern magna, or the lateral recess region with expansion in the CPA and prepontine cisterns (cerebellar ependymomas, and still more intra-brainstem ependymomas are rare). Finally, almost all cerebellar gliomas are pilocytic astrocytomas. CONCLUSIONS: A developmental and anatomic approach to the posterior fossa tumors in children (together with diffusion imaging data) provides a reliable pre-surgical identification of the tumor and of its aggressiveness.

Duration of the pre-diagnostic interval in medulloblastoma is subgroup dependent.

BACKGROUND: Children presenting with medulloblastoma have a wide range of initial presenting symptoms. However, the influence of underlying tumor biology on the initial presentation of medulloblastoma is currently unknown. In light of the recent discovery of distinct medulloblastoma subgroups, we sought to define the initial presentation of childhood medulloblastoma in a subgroup specific manner. PROCEDURE: We assembled a cohort of 126 medulloblastoma cases at the Hospital for Sick Children between 1994 and 2012 and determined subgroup affiliation using nanoString. Clinical details pertaining to the initial presentation were determined through a retrospective chart review. RESULTS: The median pre-diagnostic interval across all medulloblastoma cases was 4 weeks (IQR: 4-12 weeks). Strikingly, when the pre-diagnostic interval was then determined in a subgroup specific manner, cases with WNT and Group 4 tumors showed significantly longer median pre-diagnostic intervals of 8 weeks compared to 2 weeks for SHH and 4 weeks for Group 3 (P = 0.0001). Younger age was significantly associated with a prolonged pre-diagnostic interval (P = 0.02 for all). When stratifying by subgroup the association with age was only significant in Group 4 (P = 0.04 for Group 4). Improved survival was significantly associated with a longer pre-diagnostic interval (P = 0.02), however is no longer significant when controlling for subgroup (P = 0.07). CONCLUSIONS: The duration of the pre-diagnostic interval in childhood medulloblastoma is highly subgroup dependent, further highlighting the clinical heterogeneity and biological relevance of the four principle subgroups of medulloblastoma.

Imaging of the craniovertebral junction anomalies in children.

The craniovertebral junction (CVJ) is interposed between the unsegmented skull and the segmented spine; it is functionally unique as it allows the complex motion of the head. Because of its unique anatomy, numerous craniometric indices have been devised. Because of its complex embryology, different from that of the adjacent skull and spine, it is commonly the seat of malformations. Because of the mobility of the head, and its relative weight, the craniovertebral junction is vulnerable to trauma. Like the rest of the axial skeleton, it may be affected by many varieties of dysplasia. In addition, the bony craniovertebral junction contains the neural craniovertebral junction and its surrounding CSF: any bony instability or loss of the normal anatomic relationships may therefore compromise the neural axis. In addition, the obstruction of the meningeal spaces at this level can compromise the normal dynamics of the CSF and result in hydrocephalus and/or syringohydromyelia. To image the CVJ, plain X-rays are essentially useless. MR is optimal in depicting the soft tissues (including the neural axis) and the joints, as well as the bone itself. CT still may be important to better demonstrate the bony abnormalities.

Vertex cephaloceles: a review.

INTRODUCTION: Vertex cephaloceles (VCs), also known as midline parietal cephaloceles, are among the most common midline scalp masses. Usually composed by a meningeal wall herniating from a vertex skull defect and covered by skin, VCs may also contain both anomalous vessels and neural elements. In spite of their harmless appearance, VCs often hide complex intracranial venous and/or brain malformations so that they represent a "tip of the iceberg". Vertical embryonic positioned straight sinus, elongation of the vein of Galen, persistence of the falcine sinus, fenestration of the superior sagittal sinus, corpus callosum agenesis, intracranial cysts, tentorial malformations, cerebellar vermis agenesis, hydrocephalus, and gray matter heterotopia are some of such associated anomalies. METHODS: The treatment of VCs is surgical. It is indicated to prevent the rupture of the malformation or in case of pain or cosmetic impact. A careful preoperative radiological work up is mandatory to investigate the relationship between the VC and the sagittal sinus and/or the possible communication with the brain. The surgical procedure is usually carried out without significant complications. CONCLUSION: The prognosis of VCs is good even though the overall outcome is affected by the associated brain malformations.

Temporal and occipital lobe features in children with hypochondroplasia/FGFR3 gene mutation.

BACKGROUND: Thanatophoric dysplasia (TD) and hypochondroplasia are both caused by FGFR3 (fibroblast growth factor receptor 3) gene mutations. Temporal lobe dysplasia has been well described in thanatophoric dysplasia; however, only a couple of anecdotal cases of temporal lobe dysplasia in hypochondroplasia have been described. OBJECTIVE: To define temporal lobe abnormalities in patients with hypochondroplasia, given that they share the same genetic mutation. MATERIALS AND METHODS: We identified brain imaging studies of nine children with hypochondroplasia. The temporal lobes were assessed on CT and MRI for size and configuration of the temporal horn and aberrant sulcation of the inferior surface of the temporal lobe. RESULTS: All children had a triangular-shape temporal horn and deep transverse fissures of the inferior temporal lobe surface. Neuroimaging in our cohort revealed enlarged temporal lobes and oversulcation of the mesial temporal and occipital lobes, with abnormal inferomedial orientation of these redundant gyri. Hippocampal dysplasia was also universal. CONCLUSION: We confirmed frequent inferomesial temporal and occipital lobe abnormalities in our cohort of children with hypochondroplasia. Murine models with mutant fgfr3 display increased neuroprogenitor proliferation, cortical thickness and surface area in the temporo-occipital cortex. This is thought to result in excessive convolution and likely explains the imaging findings in this patient cohort. (Note that fgfr3 is the same genetic mutation in mice as FGFR3 is in humans.).

Diffusion tensor imaging and fiber tractography in brain malformations.

Diffusion tensor imaging (DTI) is an advanced MR technique that provides qualitative and quantitative information about the micro-architecture of white matter. DTI and its post-processing tool fiber tractography (FT) have been increasingly used in the last decade to investigate the microstructural neuroarchitecture of brain malformations. This article aims to review the use of DTI and FT in the evaluation of a variety of common, well-described brain malformations, in particular by pointing out the additional information that DTI and FT renders compared with conventional MR sequences. In addition, the relevant existing literature is summarized.

Development and dysgenesis of the cerebral cortex: malformations of cortical development.

The cerebral cortex develops in several stages from a pseudostratified epithelium at 5 weeks to an essentially complete cortex at 47 weeks. Cortical connectivity starts with thalamocortical connections in the 3rd trimester only and continues until well after birth. Vascularity adapts to proliferation and connectivity. Malformations of cortical development are classified into disorders of specification, proliferation/apoptosis, migration, and organization. However, all processes are intermingled, as for example a dysplastic cell may migrate incompletely and not connect appropriately. However, this classification is convenient for didactic purposes as long as the complex interactions between the different processes are kept in mind.

The clinicopathologic spectrum of focal cortical dysplasias: a consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission.

PURPOSE: Focal cortical dysplasias (FCD) are localized regions of malformed cerebral cortex and are very frequently associated with epilepsy in both children and adults. A broad spectrum of histopathology has been included in the diagnosis of FCD. An ILAE task force proposes an international consensus classification system to better characterize specific clinicopathological FCD entities. METHODS: Thirty-two Task Force members have reevaluated available data on electroclinical presentation, imaging, neuropathological examination of surgical specimens as well as postsurgical outcome. KEY FINDINGS: The ILAE Task Force proposes a three-tiered classification system. FCD Type I refers to isolated lesions, which present either as radial (FCD Type Ia) or tangential (FCD Type Ib) dyslamination of the neocortex, microscopically identified in one or multiple lobes. FCD Type II is an isolated lesion characterized by cortical dyslamination and dysmorphic neurons without (Type IIa) or with balloon cells (Type IIb). Hence, the major change since a prior classification represents the introduction of FCD Type III, which occurs in combination with hippocampal sclerosis (FCD Type IIIa), or with epilepsy-associated tumors (FCD Type IIIb). FCD Type IIIc is found adjacent to vascular malformations, whereas FCD Type IIId can be diagnosed in association with epileptogenic lesions acquired in early life (i.e., traumatic injury, ischemic injury or encephalitis). SIGNIFICANCE: This three-tiered classification system will be an important basis to evaluate imaging, electroclinical features, and postsurgical seizure control as well as to explore underlying molecular pathomechanisms in FCD.

Posterior fossa ependymomas: new radiological classification with surgical correlation.

PURPOSE: The key determinant of long-term outcome in infratentorial ependymomas remains the extent of surgical resection. We describe a new radiological classification system which is validated against surgical findings and correlated with risk of post-operative residual tumour. METHODS: Twenty-five consecutive patients (12 females, mean age 4.9 years, range 0.5-17 years) with infratentorial ependymomas were studied. Lesions were classified on pre-operative MRI according to the pattern of extension, brainstem displacement and involvement of the obex, as lateral-type or midfloor-type tumours. Twenty-one operative records were reviewed with respect to the microanatomical tumour origin by a paediatric neurosurgeon, blinded to MRI findings. Follow-up imaging studies were evaluated for residual tumour. RESULTS: There were 15 cases of midfloor-type tumour (anterior displacement of brainstem, infiltration of obex) and 10 cases of lateral-type tumour (lateral displacement of brainstem, obex free of tumour). Extension into prepontine or cerebellopontine cisterns was more common in lateral-type tumours. Agreement between the radiological classification and tumour origin, as defined by operative records, was seen in 18 out of 20 cases. Risk of residual tumour in lateral-type tumours was more than twice that of midfloor-type tumours (80% vs. 33%, p=0.04). Risk of tumour residual was also significantly higher when vessel encasement or prepontine extension was observed. CONCLUSIONS: Infratentorial ependymomas can be pre-operatively classified as lateral-type or midfloor-type tumours. This correlates well with operative findings. Lateral-type tumours have significantly increased risk of residual tumour compared to midfloor- type tumours and this may influence intensity of imaging surveillance.

The corpus callosum, the other great forebrain commissures, and the septum pellucidum: anatomy, development, and malformation.

There are three telencephalic commissures which are paleocortical (the anterior commissure), archicortical (the hippocampal commissure), and neocortical. In non-placental mammals, the neocortical commissural fibers cross the midline together with the anterior and possibly the hippocampal commissure, across the lamina reuniens (joining plate) in the upper part of the lamina terminalis. In placental mammals, a phylogenetically new feature emerged, which is the corpus callosum: it results from an interhemispheric fusion line with specialized groups of mildline glial cells channeling the commissural axons through the interhemispheric meninges toward the contralateral hemispheres. This concerns the frontal lobe mainly however: commissural fibers from the temporo-occipital neocortex still use the anterior commissure to cross, and the posterior occipito-parietal fibers use the hippocampal commissure, forming the splenium in the process. The anterior callosum and the splenium fuse secondarily to form the complete commissural plate. Given the complexity of the processes involved, commissural ageneses are many and usually associated with other diverse defects. They may be due to a failure of the white matter to develop or to the commissural neurons to form or to migrate, to a global failure of the midline crossing processes or to a selective failure of commissuration affecting specific commissural sites (anterior or hippocampal commissures, anterior callosum), or specific sets of commissural axons (paleocortical, hippocampal, neocortical commissural axons). Severe hemispheric dysplasia may prevent the axons from reaching the midline on one or both sides. Besides the intrinsically neural defects, midline meningeal factors may prevent the commissuration as well (interhemispheric cysts or lipoma). As a consequence, commissural agenesis is a malformative feature, not a malformation by itself. Good knowledge of the modern embryological data may allow for a good understanding of a specific pattern in a given individual patient, paving the way for better clinical correlation and genetic counseling.

Congenital spine and spinal cord malformations--self-assessment module.

The educational objectives of this self-assessment module are for the participants to exercise, self-assess, and improve their understanding of the most important features of congenital spine and spinal cord malformations.

Imaging of malformations of cortical development.

Malformations of cortical development (MCD) include a broad range of disorders that result from disruption of the major steps of cortical development: cell proliferation in germinal zones, neuronal migration and cortical organization. With the improvement and increased utilization of modern imaging techniques, MCD have been increasingly recognized as a major cause of seizure disorders. The advent of Magnetic Resonance Imaging (MRI), in particular, has revolutionized the investigation and the treatment of patients with epilepsy. High-resolution MRI may elucidate the type, the extension and the localization of MCD; therefore, in a group of patients suffering from drug-resistant partial epilepsy (DRPE), MRI greatly contributes to the identification of subjects who are suitable for surgical treatment. In the recent past, many efforts were addressed to establish the MRI diagnostic criteria for a peculiar group of MCD, namely focal cortical dysplasias (FCD), histopathologically distinguished as types I and II. Some subtle FCD, which were previously cryptic to imaging investigation, can now be recognized by MRI, however their detection and specification remains challenging. This review will re-visit the neuroimaging findings, including structural MRI, PET, co-registered PET/MRI, MEG and diffusion tensor imaging (DTI) of FCD types I and II. Three major issues will be discussed: 1) the morphological MRI features of the FCDs, 2) the utility of PET and MEG and the use of co-registration methods and 3) diffusion tensor imaging (DTI) as a future modality of investigation, which may add additional informations regarding the microstructure of the grey matter (GM) and white matter (WM) in cortical dysplasia.

Subcortical alterations in tissue microstructure adjacent to focal cortical dysplasia: detection at diffusion-tensor MR imaging by using magnetoencephalographic dipole cluster localization.

PURPOSE: To determine whether changes at diffusion-tensor magnetic resonance (MR) imaging were present in children with intractable epilepsy and focal cortical dysplasia (FCD) in (a) subcortical white matter subjacent to MR imaging-visible areas of FCD, (b) subcortical white matter beyond the MR imaging-visible abnormality but subjacent to a magnetoencephalographic (MEG) dipole cluster, and (c) deep white matter tracts. MATERIALS AND METHODS: The study protocol had institutional research ethics board approval, and written informed consent was obtained. Fifteen children with FCD and intractable epilepsy (mean age, 11.6 years; range, 3.6-18.3 years) underwent diffusion-tensor MR imaging and MEG. Regions of interest were placed in (a) the subcortical white matter subjacent to the MR imaging-visible abnormality, as well as the contralateral side; (b) the subcortical white matter beyond the MR imaging-visible abnormality but subjacent to a MEG dipole cluster, as well as the contralateral side; and (c) deep white matter tracts projecting to or from the MR imaging-visible FCD, as well as the contralateral side. Fractional anisotropy (FA), mean diffusivity, and eigenvalues (lambda(1), lambda(2), lambda(3)) were evaluated. RESULTS: Eleven of 15 children had MEG dipole clusters, and four children had MEG scatter. There were significant differences in FA, mean diffusivity, lambda(2), and lambda(3) of the subcortical white matter subjacent to the MR imaging-visible FCD (P < .001 for all), as well as that beyond the MR imaging-visible FCD but subjacent to a MEG dipole cluster (P = .001, P = .036, P < .001, and P = .002, respectively), compared with the contralateral side. There were also significant differences in FA (P < .001), mean diffusivity (P = .008), lambda(2) (P < .001), and lambda(3) (P = .001) of the deep white matter tracts projecting to or from the MR imaging-visible FCD compared with the contralateral side. CONCLUSION: With use of MEG dipole clusters to localize the epileptogenic zone, diffusion-tensor imaging can help identify alterations in tissue microstructure beyond the MR imaging-visible FCD.