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Buch ; Online ; E-Book: Handbook of Pediatric Epilepsy Case Studies, Second Edition

Montenegro, Maria Augusta / Rho, Jong M.

2023

Abstract: Research in the field of epilepsy will continue at a rapid pace, with the ultimate hope of curing many intractable epilepsy syndromes. Fully updated, this new edition is organized chronologically, from neonate through adolescence, and the handbook is ... ...

Abstract	"Research in the field of epilepsy will continue at a rapid pace, with the ultimate hope of curing many intractable epilepsy syndromes. Fully updated, this new edition is organized chronologically, from neonate through adolescence, and the handbook is the culmination of a group effort involving leading physicians and researchers whose contributions constitute a concise and practical reference for health professionals in training. Here the contributors review the recent flood of new information on the pathophysiology, genetics, and treatment of the various epilepsy syndromes and the volume is distilled into an easy-to-use guide. Fully updated text reviewing the latest research the pathophysiology, genetics, and treatment of the various epilepsy syndromes. Thorough, descriptions of the different syndromes commonly encountered in clinical practice across the pediatric range. Extensive resource section provided. Contributors describe why they chose each particular case, what they learned, and how it changed their practice. Access to a companion website, which offers digital graphics and videos on the topic"--
Schlagwörter	Epilepsy in children
Thema/Rubrik (Code)	618.92/853
Sprache	Englisch
Umfang	1 online resource (448 pages)
Ausgabenhinweis	2nd ed.
Verlag	Taylor & Francis Group
Erscheinungsort	Milton
Dokumenttyp	Buch ; Online ; E-Book
Bemerkung	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
ISBN	1-00-329647-5 ; 1-000-88525-9 ; 1-003-29647-5 ; 1-03-228358-0 ; 1-03-228354-8 ; 978-1-00-329647-8 ; 978-1-000-88525-5 ; 978-1-003-29647-8 ; 978-1-03-228358-6 ; 978-1-03-228354-8
Datenquelle	ZB MED Katalog Medizin, Gesundheit, Ernährung, Umwelt, Agrar

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Buch: Epilepsy

Rho, Jong M.

scientific foundations of clinical practice

(Neurological disease and therapy ; 64)

2004

Verfasserangabe	ed. by Jong M. Rho
Serientitel	Neurological disease and therapy ; 64
Überordnung
Sprache	Englisch
Umfang	XII, 510 S. : Ill.
Verlag	Dekker
Erscheinungsort	New York u.a.
Erscheinungsland	Vereinigte Staaten
Dokumenttyp	Buch
HBZ-ID	HT013928052
ISBN	0-8247-5043-8 ; 978-0-8247-5043-5
Datenquelle	Katalog ZB MED Medizin, Gesundheit

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Artikel ; Online: The metabolic basis of epilepsy.

Rho, Jong M / Boison, Detlev

Nature reviews. Neurology

2022 Band 18, Heft 6, Seite(n) 333–347

Abstract: The brain is a highly energy-demanding organ and requires bioenergetic adaptability to balance normal activity with pathophysiological fuelling of spontaneous recurrent seizures, the hallmark feature of the epilepsies. Recurrent or prolonged seizures ... ...

Abstract	The brain is a highly energy-demanding organ and requires bioenergetic adaptability to balance normal activity with pathophysiological fuelling of spontaneous recurrent seizures, the hallmark feature of the epilepsies. Recurrent or prolonged seizures have long been known to permanently alter neuronal circuitry and to cause excitotoxic injury and aberrant inflammation. Furthermore, pathological changes in bioenergetics and metabolism are considered downstream consequences of epileptic seizures that begin at the synaptic level. However, as we highlight in this Review, evidence is also emerging that primary derangements in cellular or mitochondrial metabolism can result in seizure genesis and lead to spontaneous recurrent seizures. Basic and translational research indicates that the relationships between brain metabolism and epileptic seizures are complex and bidirectional, producing a vicious cycle that compounds the deleterious consequences of seizures. Metabolism-based treatments such as the high-fat, antiseizure ketogenic diet have become mainstream, and metabolic substrates and enzymes have become attractive molecular targets for seizure prevention and recovery. Moreover, given that metabolism is crucial for epigenetic as well as inflammatory changes, the idea that epileptogenesis can be both negatively and positively influenced by metabolic changes is rapidly gaining ground. Here, we review evidence that supports both pathophysiological and therapeutic roles for brain metabolism in epilepsy.
Mesh-Begriff(e)	Brain/pathology ; Energy Metabolism/physiology ; Epilepsy ; Humans ; Seizures/drug therapy ; Seizures/etiology ; Status Epilepticus
Sprache	Englisch
Erscheinungsdatum	2022-03-31
Erscheinungsland	England
Dokumenttyp	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/s41582-022-00651-8
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: How does the ketogenic diet induce anti-seizure effects?

Rho, Jong M

Neuroscience letters

2017 Band 637, Seite(n) 4–10

Abstract: The high-fat ketogenic diet (KD) is a remarkably effective treatment for medically intractable epilepsy and has been part of the clinical armamentarium for nearly a century. However, the mechanisms underlying the KD's actions have remained elusive. Over ... ...

Abstract	The high-fat ketogenic diet (KD) is a remarkably effective treatment for medically intractable epilepsy and has been part of the clinical armamentarium for nearly a century. However, the mechanisms underlying the KD's actions have remained elusive. Over the past decade, there has been phenomenal international growth of clinical centers offering metabolism-based therapies for epilepsy, and rapidly expanding research into the cellular and biochemical effects induced by the KD. At present, there are many hypotheses regarding KD action, and while each is uniquely compelling, it is becoming more apparent that the KD likely works through multiple mechanisms that target fundamental biochemical pathways linked to cellular substrates (e.g., ion channels) and mediators responsible for neuronal hyperexcitability. This is not altogether surprising given the complexity of the epileptic brain, and the many different pathophysiologic mechanisms that underlie seizure genesis and epileptogenicity. The scientific literature involving the KD strongly supports the notion that epilepsy may indeed in part represent a "metabolic disease", and that this concept could serve as a novel framework for the development of more effective anti-seizure drugs.
Mesh-Begriff(e)	Animals ; Diet, High-Fat ; Diet, Ketogenic ; Humans ; Oxidative Stress/physiology ; Potassium Channels/metabolism ; Seizures/drug therapy ; Treatment Outcome
Chemische Substanzen	Potassium Channels
Sprache	Englisch
Erscheinungsdatum	2017--10
Erscheinungsland	Ireland
Dokumenttyp	Journal Article ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2015.07.034
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Metabolic epilepsies amenable to ketogenic therapies: Indications, contraindications, and underlying mechanisms.

Gavrilovici, Cezar / Rho, Jong M

Journal of inherited metabolic disease

2020 Band 44, Heft 1, Seite(n) 42–53

Abstract: Metabolic epilepsies arise in the context of rare inborn errors of metabolism (IEM), notably glucose transporter type 1 deficiency syndrome, succinic semialdehyde dehydrogenase deficiency, pyruvate dehydrogenase complex deficiency, nonketotic ... ...

Abstract	Metabolic epilepsies arise in the context of rare inborn errors of metabolism (IEM), notably glucose transporter type 1 deficiency syndrome, succinic semialdehyde dehydrogenase deficiency, pyruvate dehydrogenase complex deficiency, nonketotic hyperglycinemia, and mitochondrial cytopathies. A common feature of these disorders is impaired bioenergetics, which through incompletely defined mechanisms result in a wide spectrum of neurological symptoms, such as epileptic seizures, developmental delay, and movement disorders. The ketogenic diet (KD) has been successfully utilized to treat such conditions to varying degrees. While the mechanisms underlying the clinical efficacy of the KD in IEM remain unclear, it is likely that the proposed heterogeneous targets influenced by the KD work in concert to rectify or ameliorate the downstream negative consequences of genetic mutations affecting key metabolic enzymes and substrates-such as oxidative stress and cell death. These beneficial effects can be broadly grouped into restoration of impaired bioenergetics and synaptic dysfunction, improved redox homeostasis, anti-inflammatory, and epigenetic activity. Hence, it is conceivable that the KD might prove useful in other metabolic disorders that present with epileptic seizures. At the same time, however, there are notable contraindications to KD use, such as fatty acid oxidation disorders. Clearly, more research is needed to better characterize those metabolic epilepsies that would be amenable to ketogenic therapies, both experimentally and clinically. In the end, the expanded knowledge base will be critical to designing metabolism-based treatments that can afford greater clinical efficacy and tolerability compared to current KD approaches, and improved long-term outcomes for patients.
Mesh-Begriff(e)	Amino Acid Metabolism, Inborn Errors/diet therapy ; Animals ; Contraindications ; Diet, Ketogenic ; Energy Metabolism ; Epilepsy/diet therapy ; Humans ; Ketone Bodies/biosynthesis ; Ketone Bodies/therapeutic use ; Treatment Outcome
Chemische Substanzen	Ketone Bodies
Sprache	Englisch
Erscheinungsdatum	2020-08-11
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review
ZDB-ID	438341-2
ISSN	1573-2665 ; 0141-8955
ISSN (online)	1573-2665
ISSN	0141-8955
DOI	10.1002/jimd.12283
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: A clinically relevant selective ERK-pathway inhibitor reverses core deficits in a mouse model of autism.

Murari, Kartikeya / Abushaibah, Abdulrahman / Rho, Jong M / Turner, Ray W / Cheng, Ning

EBioMedicine

2023 Band 91, Seite(n) 104565

Abstract: Background: Extracellular signal-regulated kinase (ERK/MAPK) pathway in the brain is hypothesized to be a critical convergent node in the development of autism spectrum disorder. We reasoned that selectively targeting this pathway could reverse core ... ...

Abstract	Background: Extracellular signal-regulated kinase (ERK/MAPK) pathway in the brain is hypothesized to be a critical convergent node in the development of autism spectrum disorder. We reasoned that selectively targeting this pathway could reverse core autism-like phenotype in animal models. Methods: Here we tested a clinically relevant, selective inhibitor of ERK pathway, PD325901 (Mirdametinib), in a mouse model of idiopathic autism, the BTBR mice. Findings: We report that treating juvenile mice with PD325901 reduced ERK pathway activation, dose and duration-dependently reduced core disease-modeling deficits in sociability, vocalization and repetitive behavior, and reversed abnormal EEG signals. Further analysis revealed that subchronic treatment did not affect weight gain, locomotion, or neuronal density in the brain. Parallel treatment in the C57BL/6J mice did not alter their phenotype. Interpretation: Our data indicate that selectively inhibiting ERK pathway using PD325901 is beneficial in the BTBR model, thus further support the notion that ERK pathway is critically involved in the pathophysiology of autism. These results suggest that a similar approach could be applied to animal models of syndromic autism with dysregulated ERK signaling, to further test selectively targeting ERK pathway as a new approach for treating autism. Funding: This has beenwork was supported by Alberta Children's Hospital Research Foundation (JMR & NC), University of Calgary Faculty of Veterinary Medicine (NC), Kids Brain Health Network (NC), and Natural Sciences and Engineering Research Council of Canada (NC).
Mesh-Begriff(e)	Mice ; Animals ; Autistic Disorder/drug therapy ; Autistic Disorder/metabolism ; Autism Spectrum Disorder/metabolism ; Mice, Inbred C57BL ; MAP Kinase Signaling System ; Mice, Inbred Strains ; Disease Models, Animal
Chemische Substanzen	mirdametinib (86K0J5AK6M)
Sprache	Englisch
Erscheinungsdatum	2023-04-21
Erscheinungsland	Netherlands
Dokumenttyp	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2023.104565
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Intermittent vs continuous ketogenic diet: Impact on seizures, gut microbiota, and mitochondrial metabolism.

Shearer, Jane / Scantlebury, Morris H / Rho, Jong M / Tompkins, Thomas A / Mu, Chunlong

Epilepsia

2023 Band 64, Heft 8, Seite(n) e177–e183

Abstract: We have shown previously that the ketogenic diet (KD) is effective in reducing seizures associated with infantile spasms syndrome (ISS) and that this benefit is related to alterations in the gut microbiota. However, it remains unclear whether the ... ...

Abstract	We have shown previously that the ketogenic diet (KD) is effective in reducing seizures associated with infantile spasms syndrome (ISS) and that this benefit is related to alterations in the gut microbiota. However, it remains unclear whether the efficacy of the KD persists after switching to a normal diet. Employing a neonatal rat model of ISS, we tested the hypothesis that the impact of the KD would diminish when switched to a normal diet. Following epilepsy induction, neonatal rats were divided into two groups: continuous KD for 6 days; and a group fed with KD for 3 days and then a normal diet for 3 days. Spasms frequency, mitochondrial bioenergetics in the hippocampus, and fecal microbiota were evaluated as major readouts. We found that the anti-epileptic effect of the KD was reversible, as evidenced by the increased spasms frequency in rats that were switched from the KD to a normal diet. The spasms frequency was correlated inversely with mitochondrial bioenergetic function and a set of gut microbes, including Streptococcus thermophilus and Streptococcus azizii. These findings suggest that the anti-epileptic and metabolic benefits of the KD decline rapidly in concert with gut microbial alterations in the ISS model.
Mesh-Begriff(e)	Rats ; Animals ; Gastrointestinal Microbiome ; Diet, Ketogenic ; Seizures ; Epilepsy ; Spasms, Infantile/drug therapy ; Anticonvulsants/therapeutic use ; Spasm
Chemische Substanzen	Anticonvulsants
Sprache	Englisch
Erscheinungsdatum	2023-06-29
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/epi.17688
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Inhibition of Lactate Dehydrogenase to Treat Epilepsy.

Rho, Jong M

The New England journal of medicine

2015 Band 373, Heft 2, Seite(n) 187–189

Mesh-Begriff(e)	Animals ; Anticonvulsants/pharmacology ; Anticonvulsants/therapeutic use ; Dioxolanes/pharmacology ; Dioxolanes/therapeutic use ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Epilepsy/drug therapy ; Epilepsy/metabolism ; Humans ; L-Lactate Dehydrogenase/antagonists & inhibitors ; L-Lactate Dehydrogenase/metabolism ; Safrole/pharmacology ; Safrole/therapeutic use
Chemische Substanzen	Anticonvulsants ; Dioxolanes ; Enzyme Inhibitors ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; stiripentol (R02XOT8V8I) ; Safrole (RSB34337V9) ; isosafrole (W6337429LF)
Sprache	Englisch
Erscheinungsdatum	2015-07-09
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMcibr1503558
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Epigenetics and epilepsy prevention: The therapeutic potential of adenosine and metabolic therapies.

Boison, Detlev / Rho, Jong M

Neuropharmacology

2019 Band 167, Seite(n) 107741

Abstract: Prevention of epilepsy and its progression remains the most urgent need for epilepsy research and therapy development. Novel conceptual advances are required to meaningfully address this fundamental challenge. Maladaptive epigenetic changes, which ... ...

Abstract	Prevention of epilepsy and its progression remains the most urgent need for epilepsy research and therapy development. Novel conceptual advances are required to meaningfully address this fundamental challenge. Maladaptive epigenetic changes, which include methylation of DNA and acetylation of histones - among other mechanisms, are now well recognized to play a functional role in the development of epilepsy and its progression. The methylation hypothesis of epileptogenesis suggests that changes in DNA methylation are implicated in the progression of the disease. In this context, global DNA hypermethylation is particularly associated with chronic epilepsy. Likewise, acetylation changes of histones have been linked to epilepsy development. Clinical as well as experimental evidence demonstrate that epilepsy and its progression can be prevented by metabolic and biochemical manipulations that target previously unrecognized epigenetic functions contributing to epilepsy development and maintenance of the epileptic state. This review will discuss epigenetic mechanisms implicated in epilepsy development as well as metabolic and biochemical interactions thought to drive epileptogenesis. Therefore, metabolic and biochemical mechanisms are identified as novel targets for epilepsy prevention. We will specifically discuss adenosine biochemistry as a novel therapeutic strategy to reconstruct the DNA methylome as antiepileptogenic strategy as well as metabolic mediators, such as beta-hydroxybutyrate, which affect histone acetylation. Finally, metabolic dietary interventions (such as the ketogenic diet) which have the unique potential to prevent epileptogenesis through recently identified epigenetic mechanisms will be reviewed. This article is part of the special issue entitled 'New Epilepsy Therapies for the 21st Century - From Antiseizure Drugs to Prevention, Modification and Cure of Epilepsy'.
Mesh-Begriff(e)	Adenosine/metabolism ; Animals ; Anticonvulsants/administration & dosage ; DNA Methylation/physiology ; Diet, Ketogenic/methods ; Diet, Ketogenic/trends ; Epigenesis, Genetic/drug effects ; Epigenesis, Genetic/physiology ; Epilepsy/genetics ; Epilepsy/metabolism ; Epilepsy/therapy ; Histones/metabolism ; Humans
Chemische Substanzen	Anticonvulsants ; Histones ; Adenosine (K72T3FS567)
Sprache	Englisch
Erscheinungsdatum	2019-08-13
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2019.107741
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: A clinically relevant selective ERK-pathway inhibitor reverses core deficits in a mouse model of autismResearch in context

Kartikeya Murari / Abdulrahman Abushaibah / Jong M. Rho / Ray W. Turner / Ning Cheng

EBioMedicine, Vol 91, Iss , Pp 104565- (2023)

2023

Abstract: Summary: Background: Extracellular signal-regulated kinase (ERK/MAPK) pathway in the brain is hypothesized to be a critical convergent node in the development of autism spectrum disorder. We reasoned that selectively targeting this pathway could reverse ... ...

Abstract	Summary: Background: Extracellular signal-regulated kinase (ERK/MAPK) pathway in the brain is hypothesized to be a critical convergent node in the development of autism spectrum disorder. We reasoned that selectively targeting this pathway could reverse core autism-like phenotype in animal models. Methods: Here we tested a clinically relevant, selective inhibitor of ERK pathway, PD325901 (Mirdametinib), in a mouse model of idiopathic autism, the BTBR mice. Findings: We report that treating juvenile mice with PD325901 reduced ERK pathway activation, dose and duration-dependently reduced core disease-modeling deficits in sociability, vocalization and repetitive behavior, and reversed abnormal EEG signals. Further analysis revealed that subchronic treatment did not affect weight gain, locomotion, or neuronal density in the brain. Parallel treatment in the C57BL/6J mice did not alter their phenotype. Interpretation: Our data indicate that selectively inhibiting ERK pathway using PD325901 is beneficial in the BTBR model, thus further support the notion that ERK pathway is critically involved in the pathophysiology of autism. These results suggest that a similar approach could be applied to animal models of syndromic autism with dysregulated ERK signaling, to further test selectively targeting ERK pathway as a new approach for treating autism. Funding: : This has beenwork was supported by Alberta Children’s Hospital Research Foundation (JMR & NC), University of Calgary Faculty of Veterinary Medicine (NC), Kids Brain Health Network (NC), and Natural Sciences and Engineering Research Council of Canada (NC).
Schlagwörter	Autism ; ERK ; Selective inhibitor ; PD325901/Mirdametinib ; Repurposed drug ; EEG ; Medicine ; R ; Medicine (General) ; R5-920
Thema/Rubrik (Code)	616
Sprache	Englisch
Erscheinungsdatum	2023-05-01T00:00:00Z
Verlag	Elsevier
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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