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$The high-fat low-carbohydrate ketogenic diet (KD) is an established dietary therapy for individuals with refractory epilepsy, whose seizures are resistant to existing anti-epileptic drugs. However, use of the KD to treat refractory epilepsy is challenging because the diet is difficult for patients to implement, manage, and maintain due to its severe restrictiveness and adverse side effects. Exactly how the clinical KD reduces seizure symptoms when other anti-epileptic drugs are ineffective is poorly understood. The gut microbiome has emerged as a key intermediary between diet and host metabolism, neural activity, and behavior. The gut microbiome modulates seizure susceptibility and the anti-seizure effects of the ketogenic diet (KD) in animal models. This dissertation work seeks to understand if these relationships seen in animal models translate to KD therapies for human drug-resistant epilepsy. Herein we report that KD therapy in children with pediatric epilepsy alters the function of the human gut microbiome. In addition, colonizing mice with KD-associated human gut microbes confers increased resistance to 6-Hz psychomotor seizures, as compared to colonization with gut microbes from matched pre-treatment controls. Parallel analysis of human donor and mouse recipient metagenomic and metabolomic profiles identifies subsets of shared functional features that are seen in response to KD treatment in humans and preserved upon transfer to mice fed a standard diet. These include enriched representation of microbial genes and metabolites related to anaplerosis, fatty acid beta-oxidation, and amino acid metabolism. Mice colonized with KD-associated human gut microbes further exhibit altered hippocampal and frontal cortical transcriptomic profiles relative to colonized pre-treatment controls, including differential expression of genes related to ATP synthesis, glutathione metabolism, oxidative phosphorylation, and translation. Integrative co-occurrence network analysis of the metagenomic, metabolomic, and brain transcriptomic datasets identifies features that are shared between human and mouse networks, and select microbial functional pathways and metabolites that are candidate primary drivers of hippocampal expression signatures related to epilepsy. Together, these findings reveal key microbial functions and biological pathways that are altered by clinical KD therapies for pediatric refractory epilepsy and further linked to microbiome-induced alterations in brain gene expression and seizure protection in mice.The high-fat low-carbohydrate ketogenic diet (KD) is an established dietary therapy for individuals with refractory epilepsy, whose seizures are resistant to existing anti-epileptic drugs. However, use of the KD to treat refractory epilepsy is challenging because the diet is difficult for patients to implement, manage, and maintain due to its severe restrictiveness and adverse side effects. Exactly how the clinical KD reduces seizure symptoms when other anti-epileptic drugs are ineffective is poorly understood. The gut microbiome has emerged as a key intermediary between diet and host metabolism, neural activity, and behavior. The gut microbiome modulates seizure susceptibility and the anti-seizure effects of the ketogenic diet (KD) in animal models. This dissertation work seeks to understand if these relationships seen in animal models translate to KD therapies for human drug-resistant epilepsy. Herein we report that KD therapy in children with pediatric epilepsy alters the function of the human gut microbiome. In addition, colonizing mice with KD-associated human gut microbes confers increased resistance to 6-Hz psychomotor seizures, as compared to colonization with gut microbes from matched pre-treatment controls. Parallel analysis of human donor and mouse recipient metagenomic and metabolomic profiles identifies subsets of shared functional features that are seen in response to KD treatment in humans and preserved upon transfer to mice fed a standard diet. These include enriched representation of microbial genes and metabolites related to anaplerosis, fatty acid beta-oxidation, and amino acid metabolism. Mice colonized with KD-associated human gut microbes further exhibit altered hippocampal and frontal cortical transcriptomic profiles relative to colonized pre-treatment controls, including differential expression of genes related to ATP synthesis, glutathione metabolism, oxidative phosphorylation, and translation. Integrative co-occurrence network analysis of the metagenomic, metabolomic, and brain transcriptomic datasets identifies features that are shared between human and mouse networks, and select microbial functional pathways and metabolites that are candidate primary drivers of hippocampal expression signatures related to epilepsy. Together, these findings reveal key microbial functions and biological pathways that are altered by clinical KD therapies for pediatric refractory epilepsy and further linked to microbiome-induced alterations in brain gene expression and seizure protection in mice.$

جزئیات و درخواست

By Gregory Ryan Tadashi Lum
2023
Language: en
OTHER:OCLC:1380439596

Allgemeine Epileptologie

Das Bethel-Praxisbuch

جزئیات و درخواست

By Christian G. Bien
Publisher: Kohlhammer Verlag, 2020-12-16
Pages: 293
Language: de
ISBN_13:9783170350755
ISBN_10:3170350757
Subject: Medical

Effectiveness of the Low Glutamate Diet as an Adjunct Treatment for Pediatric Epilepsy

$Epilepsy is a chronic neurological disorder that results in seizures. About one third of patients are diagnosed with refractory epilepsy, meaning that they are unable to gain adequate seizure control through the use of anti-seizure medications. Alternative treatment options are critical for these patients, with one option being dietary therapy. The drawbacks of current dietary therapies include a range of side effects, in addition to being unable to supply all necessary nutrients. Hence, a novel dietary therapy with comparable efficacy to that of current dietary therapies that limits adverse events and increases nutrient intake would be advantageous. One potential option would be the low glutamate diet. Glutamate is the major excitatory neurotransmitter in the central nervous system. Animal models of epilepsy and brain microdialysis studies in humans with epilepsy have demonstrated elevated glutamate levels, which supports the excitation-inhibition imbalance theory of epileptogenesis. Increased blood brain barrier (BBB) permeability has also been observed in epilepsy, which in theory could allow dietary glutamate to enter the brain in higher amounts, thereby increasing seizure activity. Therefore, the current clinical trial investigated the effectiveness of the low glutamate diet as an adjunct treatment for refractory pediatric epilepsy. Patients ages 2-21 years old, with a minimum of 4 seizures per month, were recruited from the US and Canada. Participants underwent a baseline observation month, where seizure activity and 3 days of typical dietary intake were recorded. They were then randomized to the 1-month dietary intervention or 1-month wait-listed control group. Wait-listed controls continued onto the intervention diet following the 1-month wait-listed control period. During each month, families completed a seizure diary, 3-day food diary, food frequency questionnaire (FFQ), and online form, which included a Caregiver Global Impression of Change (CGIC) scale at the post diet timepoint. Measures were assessed within and between subjects (when applicable) after 1-month on the diet. Continuous variables from independent groups were assessed using a student's t-test or Mann Whitney U test, depending on normality. Related samples were assessed via paired t-tests or Wilcoxon Signed Rank tests. Categorical data were analyzed via Chi-Square or Fisher's Exact. Logistic regressions were conducted for significant bivariate analyses, with adjustments for potential confounding factors. Results indicated that there were no significant differences in percent change in seizure frequency between the diet and control groups. Pre-post diet analyses of all participants revealed that a clinical response (>50% seizure reduction) was observed in 21% of participants, 31% of caregivers reported improvement in their child's overall health based on the CGIC, and 63% of caregivers reported 9́Æ1 non-seizure improvements. Age was significantly associated with clinical response and overall health improvement at 1-month post diet. The likelihood of achieving a >50% seizure reduction decreased by 29% (0.71 [0.50-0.99], p=0.04) after adjusting for race, sex and change in food frequency questionnaire (FFQ) score. Similarly, the likelihood of achieving an overall improvement in health reduced by 29% (0.71 [0.54-0.92], p=0.01) with increasing age, after adjustment for sex, race, cognitive age, and change in FFQ score. This pilot study suggests that 1-month on the low glutamate diet may effectively reduce seizures in a small subset of pediatric epilepsy patients and may produce non-seizure improvements in a larger subset, even though the clinical efficacy of the diet does not equal that of current dietary therapies for epilepsy. Future research should evaluate longer-term exposure to this diet and the potential impact of improved micronutrient intake as compared to other dietary therapies.$

جزئیات و درخواست

By Gabrielle Sarlo
2022
Language: en
ISBN_13:9798841799504
Subject: Epilepsy in children

Der Anfallskranke in der ärztlichen Sprechstunde

جزئیات و درخواست

By Bernhard Kügelgen
1984
Pages: 191
Language: de
ISBN_10:0387129502
ISBN_13:9780387129501

Epilepsien bei Kindern und Jugendlichen

جزئیات و درخواست

By Dr. Axel Panzer, Dr. Tilman Polster, Prof. Dr. Hartmut Siemes
Publisher: Hogrefe AG, 2015-05-01
Pages: 651
Language: de
ISBN_13:9783456955131
ISBN_10:3456955138
Subject: Medical

Advances in Pediatrics 2012

جزئیات و درخواست

By Michael S. Kappy
Publisher: Mosby, 2012-07
Language: en
ISBN_10:0323088716
ISBN_13:9780323088718
Subject: Medical

Neurodivergent Youthhoods

Adolescent Rites of Passage, Disability and the Teenage Epil...

جزئیات و درخواست

By Shelda-Jane Smith
2023-08
Language: en
ISBN_10:1032217952
ISBN_13:9781032217956
Subject: Adolescence

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