3T MRI imaging approach to pediatric epileptic seizures:

Transcription

1 3T MRI imaging approach to pediatric epileptic seizures: Poster No.: C-1886 Congress: ECR 2016 Type: Educational Exhibit Authors: J. S. Alaín, E. M. DE LUCAS, J. C. Quintero Rivera, C. Pérez López, J. C. Castillo Iglesias, U. Novo ; Ourense, Ourense/ES, 2 3 Santander, Ca/ES, Ourense/ES Keywords: Seizure disorders, elearning, MR, Pediatric, Neuroradiology brain DOI: /ecr2016/C-1886 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 19

2 Learning objectives To describe the utility and indications of the 3T MRI imaging in pediatrics epileptic seizures.# To review the importance of choosing the right MRI imaging technique regarding the pediatric patient age and clinical setting.# To revise the most common causes of epileptic seizures in children by groups of age and to describe the imaging findings on 3T MRI. Background Pediatric patient suffering from epileptic seizures represent a challenging clinical population, however recent advances in 3T MRI neuroimaging continue to improve the diagnosis in many patients. Imaging protocols that include high resolution multiple sequences and multiplane adapted to patient age and clinical setting are the basis to optimize neuroimaging in epilepsy. The epileptogenic stratus causing pediatric seizures depends mainly on patient age, thus, for example, in neonatal patients the most common causes are HIE, infection, ischemia and hemorrhage, metabolism disorders, whereas in the rest of the children population focal cortical dysplasia (FCD), tuberous sclerosis (TS), neoplasm, mesial temporal sclerosis (MTS) are more frequent. Utility of the MRI in pediatric epileptic seizures -Epileptic seizure is a common and revealing clinical symptom in pediatric patients. It may point to many diverse, often severe, conditions. -MRI imaging is the most sensitive technique in the evaluation of children with suspected brain injury and especially important in neonates with seizures in which the neurologic signs are usually poor. -Some lesions are more challenging to detect, as the imaging findings can be subtle. The radiologist interpreting MRI should be familiar with the appearances of different epileptogenic substrates. MRI neuroimaging protocols in pediatric epileptic seizures Protocol recommended in pediatric patients with history of epilepsy: Page 2 of 19

3 1. Pediatric T2 FLAIR VISTA TSE T2 axial T2 FLAIR coronal (perpendicular to temporal lobe) T2 HR (1024 matrix) coronal T2* T1 IR DTI 3D T1 2. Neonates: TSE T1 TSE T2 axial and coronal T2* DTI 3D T1 T1 IR MR spectroscopy Angio MR Some considerations about the sequences to be use in children: - FLAIR: Under 24 months the FLAIR sequence may have low sensitivity and is not frequently performed. After 24 months offers excellent contrast between white and gray matter - T2 FSE: before 24 months is useful to demostrate myelin in the premature brain - 3D T1 sequence: facilitates the study of several cortical malformations. - DWI: useful to detect acute hypoxic ischemic encephalopathy in the neonate. - Additional post-processing utilizingcurvilinear reformat may help to clarify arterfactual from the true cortical thickening/blurring. The appearances of some of the epileptogenic substrate, such as FCD, may change with time, either due to brain maturation or due to seizure related changes. If a lesion is not seen on first review, it may be necessary to review the MRI again to identify subtle lesion with accurate correlation with EEG, MEG and PET findings. Fig. 11 on page 4 Page 3 of 19

4 Images for this section: Fig. 11: Fig. 11. Fifteen year-old patient with refractory partial-complex seizures and EEG: focus on right temporal region. Coronal T2 WI image show a hyperintense and swollen right hippocampus with bubbly-cystic appearance. References: HUMVSantander/Spain. Page 4 of 19

5 Findings and procedure details THE DIAGNOSES 1. MALFORMATIONS MALFOMATIONS OF CORTICAL DEVELOPMENT (MCD) -> Polymicrogyria: Fig. 1 on page 8 - Heterogeneous disorder with "too many/too small" cortical gyri - Numerous small gyri - Predilection for Sylvian fissure - Small irregular gyri, but cortex appears normal or thick on MR - T2* GRE: Hypointense foci of periventricular Ca++ # CMV Fig. 2 on page 9 - Best sequence: sagittal T1 weighted in mature brain; thin-section T2WI if unmyelinated -> Focal cortical dysplasia: Fig. 3 on page 10 - Cortical disorganization and abnormal laminar architecture - Subtle cortical-subcortical high signal - Often located at the bottom of a deep sulcus - Blurred grey/white interface - Focal cortical thickening -> Heterotopia: Fig. 4 on page 10 - Arrested migration of normal neurons along the radial path between the ventricular walls and subcortical regions - There are two types: subependymal and subcortical - Ectopic nodule or ribbon, isointense with gray matter (GM) on every MR sequence - Variable: From tiny to huge, isolated to diffuse Page 5 of 19

6 2. TUBEROUS SCLEROSIS: Inherited condition characterized by the presence of hamartomas. Fig. 5 on page 11 Key findings in the brain: 1. Cerebral tubers - Cortical/subcortical lesion expanding overlying gyrus - T2/FLAIR hyperintense, T1 hypointense after myelination - T1 hyperintense prior to myelination 2. Subependymal nodules (SENs) - Elongated nodules in locations of fetal germinal matrix - Increasing Ca++ over time % enhance 3. Subependymal giant cell astrocytoma (SEGA) - Growing nodule at caudothalamic Groove 4. White matter abnormalities 3. HYPOXIC-ISCHEMIC ENCEPHALOPATHY (HIE): Fig. 6 on page 12 - Profound HII: Low ADC in ventrolateral (VL) thalamus ± corticospinal tract (CST) in posterior limb internal capsule (PLIC) - Partial HII: VL thalamus and CST in PLIC spared, cortical injury maximal at depths of sulci - Bright DWI and # ADC occur early, even when T1WI/T2WI normal - Injuries evolve over time: DWI and ADC abnormality can # in size and severity over 1st few days due to delayed cell death; DWI and ADC normalize or # around 7-10 days 4. ERRORS OF METABOLISM: -> Glutaric Aciduria type 1: Fig. 7 on page 13 - Large sylvian fissures (from hypoplastic frontal/temporal opercula) and bright T2/FLAIR basal ganglia (caudate/putamina > globus pallidus) Page 6 of 19

7 - Acute phase: Restricted diffusion in BG on DWI images 5. CEREBROVASCULAR INJURIES: -> Germinal Matrix Hemorrhage (GMH) Fig. 8 on page 13 - Cerebral: Blood products in subependymal region, usually involving caudothalamic notch. - Cerebellar: Blood products on cerebellar surface, usually caudal. - Associated abnormalities: Hydrocephalus. -> Childhood Stroke: Fig. 9 on page 14 - Insular ribbon" sign = loss of distinction of insular cortex - Enhancement of infarcted territory typically occurs after 5-7 days - DWI (most sensitive): Diffusion restriction seen within 45 minutes of arterial occlusion 6. NEOPLASM: -> Cavernoma: Fig. 10 on page 15 - "Popcorn ball" with hemosiderin rim - T2* and SWI most sensitive due to susceptibility effect ("blooming") - Punctuated hypointense foci (black dots) on T2* - Look for associated DVA if single cavernoma -> DNET (Dysembryoplastic neuroepithelial tumor) Fig. 11 on page 16 - Swollen gyrus - Bubbly cystic appearance - May be wedge shaped and point towards the ventricle - Usually no or only little enhancement - Associated with focal cortical displasia Page 7 of 19

8 7. MESIAL TEMPORAL SCLEROSIS (MTS): Fig. 12 on page 17 - Hippocampal volume loss -> neuronal loss - atrophy - Hippocampal hyperintensity -> gliosis - seen on T2/FLAIR - In 15 % of patients another developmental abnormality can be found: frequently FCD (this is called dual pathology) 8. STURGE WEBER SYNDROME: Fig. 13 on page 17 - Atrophy mainly posteriorly - High signal on T2WI due to gliosis - Leptomeningeal enhancement -Cortical tram-track calcifications 9. CORPUS CALLOSUM DYSGENESIS: - May be complete (agenesis) or partial - Absent corpus callosum on sagittal and coronal views - Colpocephaly: dilatation of the trigones and occipital horns - Dilatated high-riding 3rd ventricle communicate with the interhemispheric - Abnormal cingulate gyrus: Radiating sulcal pattern - DTI: callosal fiber tracts from Probst bundles instead of crossing, where corpus callosum is absent - Multiple commonly associated abnormalities Images for this section: Page 8 of 19

9 Fig. 1: Fig. 2. Term neonate with congenital CMV and diffuse bilateral polymicrogyria on sagittal 3D T1 and coronal T2 images. References: HUMV-Santander/Spain. Fig. 2: Fig month-old infant. Right hemispheric polymicrogyria on coronal T2 and axial 3D T1 images. References: HUMV-Santander/Spain. Page 9 of 19

10 Fig. 3: Fig. 3. Frontal focal cortical dysplasia (red arrow) on coronal 3D T1 and T2 images. References: HUMV-Santander/Spain. Page 10 of 19

11 Fig. 4: Fig year-old infant with refractory epilepsy. Axial 3D T1 shows bilateral parieto-occipital heterotopia (red arrow). References: HUMV-Santander/Spain Page 11 of 19

12 Fig. 5: Fig. 5. Thirteen year-old patient with multifocal epilepsy. Axial T2 images shows calcified subependymal nodules (yellow arrow) and subcortical bilateral tubers (blue arrow). Sagital 3D T1 C+ shows a SEGA (red arrow). References: HUMV-Santander/ Spain. Fig. 6: Fig. 6. Preterm neonate with abruptio placentae. Bright signal on DWI and low signal on ADC map of left ventrolateral thalamus (red arrow). References: HUMVSantander/Spain. Page 12 of 19

13 Fig. 7: Fig. 7. Seven month infant with acute clinical setting of fever and seizures. Enlarged sylvian fissures and parenchymal atrophy on T2 and T1 images. Bright signal of basal ganglia on axial DWI. References: HUMV-Santander/Spain. Page 13 of 19

14 Fig. 8: Fig. 8. Premature neonate with seizures. Axial T2* shows a small focus of hypointense signal in the left caudothalamic notch due to hemorrhage with associated hydrocephalus. References: HUMV-Santander/Spain. Page 14 of 19

15 Fig. 9: Fig day-old neonate with right seizures. Axial DWI MR show corticalsubcortical temporo-parietal bright signal due to MCA territory infarction. References: HUMV-Santander/Spain. Page 15 of 19

16 Fig. 10: Fig. 10. Fifteen month-old infant with refractory seizures. Axial SWI sequence show multifocal cortical-subcortical black dots in bilateral frontal lobes due to multiple cavernomatosis. References: HUMV-Santander/Spain. Page 16 of 19

17 Fig. 11: Fig. 11. Fifteen year-old patient with refractory partial-complex seizures and EEG: focus on right temporal region. Coronal T2 WI image show a hyperintense and swollen right hippocampus with bubbly-cystic appearance. References: HUMVSantander/Spain. Fig. 12: Fig year-old patient with refractory seizures. Coronal T2 WI image show volume loss (atrophy) and high signal (gliosis) of the left side hippocampous (red arrow). References: HUMV-Santander/Spain. Page 17 of 19

18 Fig. 13: Fig year-old patient with refractory seizures. Coronal T2 WI image show volume loss (atrophy) and high signal (gliosis) of the left side hippocampous (red arrow). References: HUMV-Santander/Spain. Fig. 14: Fig. 14. Term neonate with Down syndrome. Sagittal and coronal 3D T1 shows dysgenesis (agenesis) of callosum corpus. References: References: HUMV-Santander/ Spain. Page 18 of 19

19 Conclusion The MRI is an essential tool in detecting brain alterations causing insurmountable child seizures and should always be interpreted according to EEG findings. The accuracy of MRI in the study of seizures depends on a suitable imaging technique, with excellent anatomic resolution and adapted to the patient's age and clinic status, which will bring the necessary information for a correct diagnosis. The Hypoxic-ischemic encephalopathy is the most common cause of seizures in infants, while in the rest of the children focal cortical dysplasia (DCF) is more common; regarding teenagers (the same for adults) mesial temporal sclerosis (MTS) is the most common cause. Personal information References 1. Girard N, Raybaud Ch. Neonates with Seizures: What to consider, How to Image. Magn Reson Imaginf Clin N Am 19 (2011) Rastogi S, Lee Ch, Salamon N. Neuroimaging in Pediatric Epilepsy: A Multimodality Approach. Radiographics 2008; 28: Daghistani R, Widjaja E. Role of MRI in patient selection for surgical treatment of intractable epilepsy in infancey. Brain & Deleopment 35 (2013) Vattipally V R, Bronen R A. MR Imaging of Epilepsy: Strategies for Successful Interpretation. Radiol Clin N Am 44 (2006) Page 19 of 19