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Rolandic Epilepsy

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1. Rare gene deletions in genetic generalized and Rolandic epilepsies. (PubMed)

Rare gene deletions in genetic generalized and Rolandic epilepsies. Genetic Generalized Epilepsy (GGE) and benign epilepsy with centro-temporal spikes or Rolandic Epilepsy (RE) are common forms of genetic epilepsies. Rare copy number variants have been recognized as important risk factors in brain disorders. We performed a systematic survey of rare deletions affecting protein-coding genes derived from exome data of patients with common forms of genetic epilepsies. We analysed exomes from 390 (...) European patients (196 GGE and 194 RE) and 572 population controls to identify low-frequency genic deletions. We found that 75 (32 GGE and 43 RE) patients out of 390, i.e. ~19%, carried rare genic deletions. In particular, large deletions (>400 kb) represent a higher burden in both GGE and RE syndromes as compared to controls. The detected low-frequency deletions (1) share genes with brain-expressed exons that are under negative selection, (2) overlap with known autism and epilepsy-associated candidate

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2018 PLoS ONE

2. Identification of new risk factors for rolandic epilepsy: CNV at Xp22.31 and alterations at cholinergic synapses

Identification of new risk factors for rolandic epilepsy: CNV at Xp22.31 and alterations at cholinergic synapses Identification of new risk factors for rolandic epilepsy: CNV at Xp22.31 and alterations at cholinergic synapses | JMG Contact blog by Rolandic epilepsy (RE) is the most common genetic childhood epilepsy, with focal nocturnal seizures and neurodevelopmental impairments. In this study of 186 children with RE from ethnically diverse populations, we identified rare copy number variation (...) (CNV, large duplications or deletions of DNA) in 84. Children with RE carried CNVs that disrupt genes known to cause other types of epilepsy (e.g. KCTD7 , ARHGEF15) and other developmental disorders, as well as genes involved in development of the brain. Some children also carried CNV at regions of the genome called hotspots, especially Xp22.31. Our results uncover new areas of research focus, and emphasise the importance of studying non-western-European populations to uncover a full picture

2018 JMG Contact blog

3. Stridor as initial presentation of rolandic epilepsy. (PubMed)

Stridor as initial presentation of rolandic epilepsy. The authors present the case of a 5-year-old girl referred to our institution due to several episodes of nocturnal stridor with ocular retroversion and parental notion of apnea. She has been previously submitted to adenotonsillectomy. Due to symptoms worsening she was referred to our hospital. Here, a nasal fiberoptic endoscopy evaluation was conducted and a diagnosis of laryngomalacia was done. The was submitted to CO2 laser

2019 International Journal of Pediatric Otorhinolaryngology

4. Exome-wide analysis of mutational burden in patients with typical and atypical Rolandic epilepsy. (PubMed)

Exome-wide analysis of mutational burden in patients with typical and atypical Rolandic epilepsy. Rolandic epilepsy (RE) is the most common focal epilepsy in childhood. To date no hypothesis-free exome-wide mutational screen has been conducted for RE and atypical RE (ARE). Here we report on whole-exome sequencing of 194 unrelated patients with RE/ARE and 567 ethnically matched population controls. We identified an exome-wide significantly enriched burden for deleterious and loss-of-function

2018 European Journal of Human Genetics

5. Rolandic Epilepsy Genomewide Association International Study

Rolandic Epilepsy Genomewide Association International Study Rolandic Epilepsy Genomewide Association International Study - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Rolandic Epilepsy Genomewide (...) Summary: We have discovered a small change in the genetic code which increases the risk of the brainwave abnormality that is found in rolandic epilepsy. We now wish to confirm this using a second much larger sample of patients. We will investigate the other genetic changes that cause people with the brainwave abnormality to develop seizures, as well as problems with speech, coordination, attention and learning. Condition or disease Intervention/treatment Rolandic Epilepsy Other: Blood draw Other

2018 Clinical Trials

6. Tantrums, Emotion Reactions and Their EEG Correlates in Childhood Benign Rolandic Epilepsy vs. Complex Partial Seizures: Exploratory Observations (PubMed)

Tantrums, Emotion Reactions and Their EEG Correlates in Childhood Benign Rolandic Epilepsy vs. Complex Partial Seizures: Exploratory Observations We explored associations between EEG pathophysiology and emotional/behavioral (E/B) problems of children with two types of epilepsy using standard parent questionnaires and two new indicators: tantrums recorded by parents at home and brief, emotion-eliciting situations in the laboratory. Children with Benign Rolandic epilepsy (BRE, N = 6) reportedly (...) reactions. Such EEG abnormalities in left hemisphere correlated with greater social fear, right hemisphere EEG abnormalities with greater anger. Right hemisphere localization in CPS was also associated with parent-reported problems at home. If epilepsy alters neural circuitry thereby increasing negative emotions, additional assessment of anti-epileptic drug treatment of epilepsy-related E/B problems would be warranted.

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2018 Frontiers in behavioral neuroscience

7. Identification of new risk factors for rolandic epilepsy: CNV at Xp22.31 and alterations at cholinergic synapses. (PubMed)

Identification of new risk factors for rolandic epilepsy: CNV at Xp22.31 and alterations at cholinergic synapses. Rolandic epilepsy (RE) is the most common genetic childhood epilepsy, consisting of focal, nocturnal seizures and frequent neurodevelopmental impairments in speech, language, literacy and attention. A complex genetic aetiology is presumed in most, with monogenic mutations in GRIN2A accounting for >5% of cases.To identify rare, causal CNV in patients with RE.We used high-density SNP (...) patients with RE carried a rare CNV that disrupted genes associated with other epilepsies (KCTD7, ARHGEF15, CACNA2D1, GRIN2A and ARHGEF4), and 17 cases carried CNVs that disrupted genes associated with other neurological conditions or that are involved in neuronal signalling/development. Network analysis of disrupted genes with high brain expression identified significant enrichment in pathways of the cholinergic synapse, guanine-exchange factor activation and the mammalian target of rapamycin.Our

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2018 Journal of Medical Genetics

8. Reading comprehension difficulties in children with rolandic epilepsy. (PubMed)

Reading comprehension difficulties in children with rolandic epilepsy. Difficulties in reading comprehension can arise from either word reading or listening comprehension difficulties, or a combination of the two. We sought to determine whether children with rolandic epilepsy had poor reading comprehension relative to typically developing comparison children, and whether such difficulties were associated with word reading and/or general language comprehension difficulties.In this cross (...) -sectional study, children with rolandic epilepsy (n=25; 16 males, 9 females; mean age 9y 1mo, SD 1y 7mo) and a comparison group (n=39; 25 males, 14 females; mean age 9y 1mo, SD 1y 3mo) completed assessments of reading comprehension, listening comprehension, word/non-word reading, speech articulation, and Non-verbal IQ.Reading comprehension and word reading were worse in children with rolandic epilepsy (F1,61 =6.89, p=0.011, ηp2=0.10 and F1,61 =6.84, p=0.011, ηp2=0.10 respectively), with listening

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2017 Developmental Medicine and Child Neurology

9. Benign Rolandic epilepsy presenting like paradoxical vocal fold motion. (PubMed)

Benign Rolandic epilepsy presenting like paradoxical vocal fold motion. Paradoxical vocal fold motion (PVFM) is characterized by vocal fold adduction during respiration. Benign Rolandic epilepsy (BRE) is the most common childhood epilepsy and can cause oropharyngolaryngeal or facial manifestations. A 9-year-old male presented with intermittent apnea lasting 30-60 seconds and presumed PVFM. The patient's physical and fiberoptic exam were normal. He was admitted and found to have episodes (...) of oxygen desaturation, neck twitching, and tongue burning. An EEG revealed focal epilepsy. After starting anti-epileptic medications, he had resolution of symptoms. Our patient was eventually diagnosed with BRE, a focal onset epilepsy that can mimic primary otolaryngologic disease.Copyright © 2017 Elsevier B.V. All rights reserved.

2017 International Journal of Pediatric Otorhinolaryngology

10. [Cognitive Development in Children with Benign Rolandic Epilepsy of Childhood with Centrotemporal Spikes - Results of a Current Systematic Database Search].

[Cognitive Development in Children with Benign Rolandic Epilepsy of Childhood with Centrotemporal Spikes - Results of a Current Systematic Database Search]. Benign Rolandic Epilepsy (BRE) is one of the most common epilepsy syndromes in childhood. Although global intellectual performance is typically normal in BRE-patients, problems were found in specific cognitive domains. To summarize recent empirical findings concerning cognitive development in children with BRE a systematic literature search

2017 Fortschritte der Neurologie-Psychiatrie

11. Is a microRNA‐328 binding site in PAX6 associated with Rolandic epilepsy? (PubMed)

Is a microRNA‐328 binding site in PAX6 associated with Rolandic epilepsy? 28382309 2018 11 13 2328-9503 4 4 2017 04 Annals of clinical and translational neurology Ann Clin Transl Neurol Is a microRNA-328 binding site in PAX6 associated with Rolandic epilepsy? 276-277 10.1002/acn3.401 McGlade Amelia A Epilepsy Research Centre Department of Medicine University of Melbourne Austin Health Heidelberg Victoria 3084 Australia. Myers Kenneth A KA Epilepsy Research Centre Department of Medicine (...) University of Melbourne Austin Health Heidelberg Victoria 3084 Australia. Berkovic Samuel F SF Epilepsy Research Centre Department of Medicine University of Melbourne Austin Health Heidelberg Victoria 3084 Australia. Scheffer Ingrid E IE Epilepsy Research Centre Department of Medicine University of Melbourne Austin Health Heidelberg Victoria 3084 Australia; Florey Institute and Department of Paediatrics University of Melbourne Royal Children's Hospital Parkville Victoria 3052 Australia. Petrovski Slavé S

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2017 Annals of clinical and translational neurology

12. Reply to: Is a microRNA‐328 binding site in PAX6 associated with Rolandic epilepsy? (PubMed)

Reply to: Is a microRNA‐328 binding site in PAX6 associated with Rolandic epilepsy? 28382310 2019 01 11 2328-9503 4 4 2017 04 Annals of clinical and translational neurology Ann Clin Transl Neurol Reply to: Is a microRNA-328 binding site in PAX6 associated with Rolandic epilepsy? 278-280 10.1002/acn3.403 Strug Lisa J LJ The Centre for Applied Genomics and Program in Genetics and Genome Biology The Hospital for Sick Children Toronto Ontario Canada; Division of Biostatistics and Department

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2017 Annals of clinical and translational neurology

13. Ripples on rolandic spikes: A marker of epilepsy severity. (PubMed)

Ripples on rolandic spikes: A marker of epilepsy severity. Children with rolandic spikes may or may not have seizures, ranging from benign rolandic epilepsy to severe atypical rolandic epilepsy. We investigated whether ripples (80-250 Hz), superimposed on rolandic spikes in surface electroencephalography (EEG), can differentiate between different entities.In this cohort study we analyzed the EEG studies of children with rolandic spikes without other EEG or magnetic resonance imaging (MRI (...) ) abnormalities. They were divided into the following three groups: (1) rolandic spikes but no epilepsy, (2) typical rolandic epilepsy, and (3) atypical and symptomatic rolandic epilepsy. Ripples superimposed on rolandic spikes were marked in 10 minutes of EEG, and compared to the number of seizures before the EEG. Receiver operating characteristic (ROC) curves were constructed to determine the predictive value of ripples and spikes for having epilepsy (groups 2 and 3) and for differentiating benign courses

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2016 Epilepsia

14. Rolandic Epilepsy

Rolandic Epilepsy Rolandic Epilepsy Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Rolandic Epilepsy Rolandic Epilepsy Aka: Rolandic (...) Epilepsy From Related Chapters II. Epidemiology Onset in mid-childhood of Rolandic : 25% of cases Occurs more in males III. Symptoms Nocturnal Begins in face Variable generalization to tonic-clonic May present as IV. Signs Normal exam Normal intelligence V. Diagnosis: Electroencephalogram (EEG) Centrotemporal spikes Usually unilateral involvement VI. Management: Prophylaxis Reserve prophylaxis if possible VII. Course Majority of patients are -free after 5 years Images: Related links to external sites

2018 FP Notebook

15. Real-time effects of centrotemporal spikes on cognition in rolandic epilepsy: An EEG-fMRI study. (PubMed)

Real-time effects of centrotemporal spikes on cognition in rolandic epilepsy: An EEG-fMRI study. To identify the real-time effects of interictal rolandic spikes (or centrotemporal spikes [CTS]) on language, behavior, and cognitive function in patients with rolandic epilepsy (RE).We studied 22 medication-naive patients with RE using EEG-fMRI with a 3T MRI scanner. We used simultaneous EEG to define the pre-CTS, CTS, and post-CTS periods. We analyzed the dynamic functional connectivity maps (...) of the rolandic network during the 3 interictal CTS periods.The analysis of dynamic changes revealed positive correlations between the bilateral rolandic areas and the left inferior frontal gyrus (IFG; Broca area), the left inferior parietal lobe and the supramarginal gyrus (areas responsible for receptive language function), and the right IFG and left caudate. Anti-correlations were found in the default mode network (bilateral superior frontal gyrus, left middle frontal gyrus, left middle temporal gyrus

2016 Neurology

16. A microRNA‐328 binding site in PAX6 is associated with centrotemporal spikes of rolandic epilepsy (PubMed)

A microRNA‐328 binding site in PAX6 is associated with centrotemporal spikes of rolandic epilepsy Rolandic epilepsy is a common genetic focal epilepsy of childhood characterized by centrotemporal sharp waves on electroencephalogram. In previous genome-wide analysis, we had reported linkage of centrotemporal sharp waves to chromosome 11p13, and fine mapping with 44 SNPs identified the ELP4-PAX6 locus in two independent US and Canadian case-control samples. Here, we aimed to find a causative (...) variant for centrotemporal sharp waves using a larger sample and higher resolution genotyping array.We fine-mapped the ELP4-PAX6 locus in 186 individuals from rolandic epilepsy families and 1000 population controls of European origin using the Illumina HumanCoreExome-12 v1.0 BeadChip. Controls were matched to cases on ethnicity using principal component analysis. We used generalized estimating equations to assess association, followed up with a bioinformatics survey and literature search to evaluate

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2016 Annals of clinical and translational neurology

17. Diagnosis and management of epilepsy in adults

Diagnosis and management of epilepsy in adults SIGN 143 • Diagnosis and management of epilepsy in adults A national clinical guideline Evidence May 2015 · Revised 2018KEY TO EVIDENCE STATEMENTS AND GRADES OF RECOMMENDATIONS LEVELS OF EVIDENCE 1 ++ High-quality meta-analyses, systematic reviews of RCTs, or RCTs with a very low risk of bias 1 + Well-conducted meta-analyses, systematic reviews, or RCTs with a low risk of bias 1 - Meta-analyses, systematic reviews, or RCTs with a high risk of bias (...) in the web version of this document, which is the definitive version at all times. This version can be found on our web site www.sign.ac.uk. This document is produced from elemental chlorine-free material and is sourced from sustainable forests.Scottish Intercollegiate Guidelines Network Diagnosis and management of epilepsy in adults A national clinical guideline Revised 2018Scottish Intercollegiate Guidelines Network Gyle Square, 1 South Gyle Crescent Edinburgh EH12 9EB www.sign.ac.uk First published

2018 SIGN

18. Antiepileptic drug treatment of rolandic epilepsy and Panayiotopoulos syndrome: clinical practice survey and clinical trial feasibility. (PubMed)

Antiepileptic drug treatment of rolandic epilepsy and Panayiotopoulos syndrome: clinical practice survey and clinical trial feasibility. The evidence base for management of childhood epilepsy is poor, especially for the most common specific syndromes such as rolandic epilepsy (RE) and Panayiotopoulos syndrome (PS). Considerable international variation in management and controversy about non-treatment indicate the need for high quality randomised controlled trials (RCT). The aim of this study (...) is, therefore, to describe current UK practice and explore the feasibility of different RCT designs for RE and PS.We conducted an online survey of 590 UK paediatricians who treat epilepsy. Thirty-two questions covered annual caseload, investigation and management practice, factors influencing treatment, antiepileptic drug preferences and hypothetical trial design preferences.132 responded (22%): 81% were paediatricians and 95% at consultant seniority. We estimated, annually, 751 new RE cases and 233 PS

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2015 Archives of Disease in Childhood

19. Risk factors for reading disability in rolandic epilepsy families (PubMed)

Risk factors for reading disability in rolandic epilepsy families The high prevalence and impact of neurodevelopmental comorbidities in childhood epilepsy are now well known, as are the increased risks and familial aggregation of reading disability (RD) and speech sound disorder (SSD) in rolandic epilepsy (RE). The risk factors for RD in the general population include male sex, SSD, and ADHD, but it is not known if these are the same in RE or whether there is a contributory role of seizure (...) risk factors for RD in RE are SSD, ADHD, and male sex, the same risk factors as for RD without epilepsy. Seizure or treatment variables do not appear to be important risk factors for RD in probands with RE, and there was no evidence to support interictal EEG focal sharp waves as a risk factor for RD in siblings. Future studies should focus on the precise neuropsychological characterization of RD in families with RE and on the effectiveness of standard oral-language and reading

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2015 Epilepsy & behavior : E&B

20. Regaining White Matter Integrity and Neurocognitive Development in Rolandic Epilepsy After the Storm (PubMed)

Regaining White Matter Integrity and Neurocognitive Development in Rolandic Epilepsy After the Storm 25678881 2015 02 14 2018 11 13 1535-7597 15 1 2015 Jan-Feb Epilepsy currents Epilepsy Curr Regaining white matter integrity and neurocognitive development in rolandic epilepsy after the storm. 20-3 10.5698/1535-7597-15.1.20 Rossi Marvin A MA eng Journal Article United States Epilepsy Curr 101135954 1535-7511 2015 2 14 6 0 2015 2 14 6 0 2015 2 14 6 1 ppublish 25678881 10.5698/1535-7597-15.1.20 (...) PMC4320951 AJNR Am J Neuroradiol. 2003 Oct;24(9):1857-62 14561616 Epilepsy Res. 2013 Mar;104(1-2):105-11 23182414 Epilepsy Res. 2005 Jul;65(3):137-46 16043327 Neurology. 2001 Aug 14;57(3):537-9 11502931 Epilepsy Res. 2010 Feb;88(2-3):208-14 20044239 Magn Reson Imaging. 2002 Sep;20(7):511-9 12413596 Epilepsy Res. 2007 Jun;75(1):57-62 17531444 Neurology. 2014 Apr 1;82(13):1162-6 24562059 Neurology. 1999 Mar 23;52(5):1021-7 10102423 Epilepsy Res. 2012 May;99(3):267-73 22227509 Neuroimage. 2005 Nov 15;28(3

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2015 Epilepsy Currents

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