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Libros sobre el tema "Experimental epilepsy"

Autor: Grafiati
Publicado: 11 de marzo de 2023

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1

D, Schmidt Dieter M., Morselli Paolo Lucio, World Health Organization, International League against Epilepsy y Workshop on Intractable Epilepsy (1985 : Saint-Germain-en-Laye, France), eds. Intractable epilepsy: Experimental and clinical aspects. New York: Raven Press, 1986.

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2

Alain, Malafosse, ed. Idiopathic generalized epilepsies: Clinical, experimental and genetic aspects. London: John Libbey, 1994.

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3

G, Bazán Nicholás, ed. Lipid mediators in ischemic brain damage and experimental epilepsy. Basel: Karger, 1990.

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4

Vohora, Divya, ed. Experimental and Translational Methods to Screen Drugs Effective Against Seizures and Epilepsy. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1254-5.

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5

Corcoran, Michael E. y Gordon Campbell Teskey. Kindling: An Inquiry into Experimental Epilepsy. Oxford University Press, 2004.

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6

Shaikh, Mohd Farooq, Ayanabha Chakraborti, Annamaria Vezzani y Jafri Malin Abdullah, eds. Experimental Models of Epilepsy and Related Comorbidities. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-843-1.

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7

Shaikh, Mohd Farooq, Teresa Ravizza, Jafri Malin Abdullah, Ayanabha Chakraborti y Terence John O’Brien, eds. Experimental & Clinical Epilepsy and Related Comorbidities. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-146-6.

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8

(Editor), Devin K. Binder y Helen E. Scharfman (Editor), eds. Recent Advances in Epilepsy Research (Advances in Experimental Medicine and Biology). Springer, 2004.

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9

Schmidt, Dieter. Intractable Epilepsy: Experimental and Clinical Aspects (L.E.R.S. Monograph Series, Vol 5/Order No 1684). Raven Pr, 1987.

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10

Vohora, Divya. Experimental and Translational Methods to Screen Drugs Effective Against Seizures and Epilepsy. Springer, 2022.

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11

Vohora, Divya. Experimental and Translational Methods to Screen Drugs Effective Against Seizures and Epilepsy. Springer, 2021.

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12

Rho, Jong M. Overview. Editado por Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0011.

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After nearly a century of clinical use, the ketogenic diet is firmly established as an efficacious treatment for medically intractable epilepsy. Intriguingly, there is growing experimental evidence that the ketogenic diet and its metabolites also render neuroprotective and potentially disease-modifying effects. Hence, dietary and metabolic therapies have been attempted in a variety of neurological disorders other than epilepsy, including brain cancer, cognitive disorders, autism, neurotrauma, pain, and multiple sclerosis. This section, “Ketogenic Diet: Emerging Clinical Applications and Future Potential,” explores the current preclinical and clinical evidence for metabolism-based treatments designed to counter the myriad disease processes seen in many neurological conditions. Specific attention has been given to the effects of the ketogenic diet in malignant brain cancer, autism spectrum disorder, Alzheimer’s disease, traumatic brain and spinal cord injury, pain, and multiple sclerosis.
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13

Dupuis, Nina y Stéphane Auvin. Anti-Inflammatory Effects of a Ketogenic Diet. Editado por Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0017.

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The high-fat, low-carbohydrate ketogenic diet (KD) is an established and proven treatment for pharmacoresistant epilepsy. Recently, the KD is being explored for some inflammation-induced epileptic encephalopathies. Given the broad neuroprotective properties of the KD in various experimental models of neurological disorders, there are yet additional potential future uses. Consistent with this, there is growing evidence that the KD exerts anti-inflammatory activity. Ketone bodies, caloric restriction, and polyunsaturated fatty acids might be involved in the modulation of inflammation by the KD. This chapter reviews the evidence that, in part through anti-inflammatory effects, the KD holds promise in the treatment of certain epileptic disorders, neuropathic pain, multiple sclerosis, and Parkinson’s disease.
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14

Stafstrom, Carl E. Dietary Therapy for Neurological Disorders. Editado por Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0018.

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Dietary and metabolic therapies such as the high-fat, low-carbohydrate ketogenic diet (KD) are best known for the treatment of intractable epilepsy. Yet, dietary and metabolic approaches have also found some efficacy in a wide variety of other neurological diseases, including autism spectrum disorder, brain trauma, Alzheimer’s disease, sleep disorders, brain tumors, pain, and multiple sclerosis, as discussed in other chapters of this volume. This chapter provides an overview of clinical and experimental studies using the KD in an array of other neurologic disorders: amyotrophic lateral sclerosis, Parkinson’s disease, mood disorders, and migraine. Despite the wide spectrum of pathophysiological mechanisms underlying these disorders, it is possible that one or more final common metabolic pathways might be influenced by dietary intervention. There is compelling albeit preliminary evidence that correction of aberrant energy metabolism through dietary manipulation could favorably influence diverse neurological diseases.
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15

Kawamura, Masahito. Ketogenic Diet in a Hippocampal Slice. Editado por Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0021.

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The hippocampus is thought to be a good experimental model for investigating epileptogenesis in and/or antiepileptic therapy for temporal lobe epilepsy. The hippocampus is also a useful target for researching the ketogenic diet. This chapter focuses on electrophysiological recordings using hippocampal slices and introduces their use for studying the anticonvulsant effects underlying ketogenic diets. The major difficulty in using hippocampal slices is the inability to precisely reproduce the in vivo condition of ketogenic diet feeding in this in vitro preparation. Three different approaches are reported to reproduce diet effects in the hippocampal slices: (1) direct application of ketone bodies, (2) mimicking the ketogenic diet condition with whole-cell patch-clamp technique, and (3) hippocampal slices from ketogenic diet–fed animals. Significant results have been found with each of these methods. These three approaches are useful tools to elucidate the underlying anticonvulsant mechanisms of the ketogenic diet.
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16

Rotenberg, Alexander, Alvaro Pascual-Leone y Alan D. Legatt. Transcranial Electrical and Magnetic Stimulation. Editado por Donald L. Schomer y Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0028.

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Noninvasive magnetic and electrical stimulation of cerebral cortex is an evolving field. The most widely used variant, transcranial electrical stimulation (TES), is routinely used for intraoperative monitoring. Transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) are emerging as clinical and experimental tools. TMS has gained wide acceptance in extraoperative functional cortical mapping. TES and TMS rely on pulsatile stimulation with electrical current intensities sufficient to trigger action potentials within the stimulated cortical volume. tDCS, in contrast, is based on neuromodulatory effects of very-low-amplitude direct current conducted through the scalp. tDCS and TMS, particularly when applied in repetitive trains, can modulate cortical excitability for prolonged periods and thus are either in active clinical use or in advanced stages of clinical trials for common neurological and psychiatric disorders such as major depression and epilepsy. This chapter summarizes physiologic principles of transcranial stimulation and clinical applications of these techniques.
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17

Cheng, Ning, Susan A. Masino y Jong M. Rho. Metabolic Therapy for Autism Spectrum Disorder and Comorbidities. Editado por Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0014.

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Autism spectrum disorder (ASD) is a heretogenous developmental disorder characterized by deficits in sociability and communication and by repetitive and/or restrictive behaviors. Currently, only comorbid manifestations can be alleviated (such as seizures and sleep disturbance) not core behavioral symptoms. Recent studies have increasingly implicated mitochondrial dysfunction as a cause of ASD. Mitochondria play an integral role in many cellular functions and are susceptible to many pathophysiological insults. Derangements in mitochondrial structure and function provide a scientific rationale for experimental therapeutics. Meanwhile, the high-fat, low-carbohydrate ketogenic diet (KD) has been shown to enhance mitochondrial function through a multiplicity of mechanisms. Reviewed herein is clinical and basic laboratory evidence for the use of metabolism-based therapies such as the KD in the treatment of ASD, as well as emerging comorbid models of epilepsy and autism. Future research directions aimed at validating such therapeutic approaches and identifying novel mechanistic targets are discussed.
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18

Anderson, James A. The Brain Doesn’t Work by Logic. Oxford University Press, 2018. http://dx.doi.org/10.1093/acprof:oso/9780199357789.003.0008.

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This chapter gives three examples of real neural computation. The conclusion is that the “brain doesn’t work by logic.” First, is the Limulus (horseshoe crab) lateral eye. The neural process of “lateral inhibition” tunes the neural response of the compound eye to allow crabs to better see other crabs for mating. Second, the retina of the frog contains cells that are selective to specific properties of the visual image. The frog responds strongly to the moving image of a bug with one class of selective retinal receptors. Third, experiments on patients undergoing neurosurgery for epilepsy found single neurons in several cortical areas that were highly selective to differing images, text strings, and spoken names of well-known people. In addition, new selective responses could be formed quickly. The connection to concepts in cognitive science seems inevitable. One possible mechanism is through associatively linked “cell assemblies.”
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19

Permanent Present Tense The Man With No Memory And What He Taught The World. Penguin Books Ltd, 2013.

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20

Zeidman, Lawrence A. Brain Science under the Swastika. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198728634.001.0001.

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Eighty years ago the greatest mass murder of human beings of all time occurred in Nazi occupied Europe. This began with the mass extermination of patients with neurologic and psychiatric disorders that rendered them “useless eaters” to Hitler’s regime. The neuropsychiatric profession was systematically “cleansed” beginning in 1933, but racism and eugenics had infiltrated the specialty in the decades before that. With the installation of Nazi-principled neuroscientists, mass forced sterilization was enacted, which slowed down by the start of World War II and the advent of patient murder. But the murder of roughly 275,000 patients by the end of the war was not enough. The patients’ brains and neurologic body parts were stored and used in scientific publications both during and long after the war. Also, patients themselves were used in unethical ways for epilepsy and multiple sclerosis experiments. Relatively few neuroscientists resisted the Nazis, with some success in the occupied countries. Most neuroscientists involved in unethical actions continued their careers unscathed after the war. Few answered for their actions in a professional or criminal sense, and few repented. The legacy of such a depraved era in the history of neuroscience and medical ethics is that codes exist by which patients and research subjects are protected from harm. But this protection is possibly subject to political extremes and only by understanding the horrible past can our profession police itself. Individual neuroscientists can protect patients and colleagues if they are aware of the dangers of a utilitarian, unethical, and uncompassionate mindset.
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