Modulation of Glucose Availability and Effects of Hypo- and Hyperglycemia on Status Epilepticus: What We Do Not Know Yet
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Modulation of Glucose Availability and Effects of Hypoand Hyperglycemia on Status Epilepticus: What We Do Not Know Yet? Igor Santana de Melo 1 & Amanda Larissa Dias Pacheco 1 & Yngrid Mickaelli Oliveira dos Santos 1 & Laura Mello Figueiredo 1 & Dannyele Cynthia Santos Pimentel Nicacio 1 & Leia Cardoso-Sousa 2 & Marcelo Duzzioni 1 & Daniel Leite Góes Gitaí 1 & Cristiane Queixa Tilelli 3 & Robinson Sabino-Silva 2 & Olagide Wagner de Castro 1 Received: 3 August 2020 / Accepted: 14 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Status epilepticus (SE) can lead to serious neuronal damage and act as an initial trigger for epileptogenic processes that may lead to temporal lobe epilepsy (TLE). Besides promoting neurodegeneration, neuroinflammation, and abnormal neurogenesis, SE can generate an extensive hypometabolism in several brain areas and, consequently, reduce intracellular energy supply, such as adenosine triphosphate (ATP) molecules. Although some antiepileptic drugs show efficiency to terminate or reduce epileptic seizures, approximately 30% of TLE patients are refractory to regular antiepileptic drugs (AEDs). Modulation of glucose availability may provide a novel and robust alternative for treating seizures and neuronal damage that occurs during epileptogenesis; however, more detailed information remains unknown, especially under hypo- and hyperglycemic conditions. Here, we review several pathways of glucose metabolism activated during and after SE, as well as the effects of hypo- and hyperglycemia in the generation of self-sustained limbic seizures. Furthermore, this study suggests the control of glucose availability as a potential therapeutic tool for SE. Keywords Glucose . Hypometabolism . Hypoglycemia . Hyperglycemia . Status epilepticus . Epilepsy
Introduction Status epilepticus (SE) is a clinical emergency characterized by either a continuous self-sustained seizure or a sequence of short seizures with no return to baseline, unleashing a high mortality rate [1–8]. SE can be convulsive or nonconvulsive [9–16], and it is capable of promoting neuronal death, gliosis,
* Robinson Sabino-Silva [email protected] * Olagide Wagner de Castro [email protected] 1
Department of Physiology, Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Av. Lourival de Melo Mota, km 14, Campus A. C. Simões, Cidade Universitária, Maceió, AL CEP 57072-970, Brazil
2
Department of Physiology, Institute of Biomedical Sciences, Federal University of Uberlandia (UFU), ARFIS, Av. Pará, 1720, Campus Umuruama, Uberlandia, MG CEP 38400-902, Brazil
3
Physiology Laboratory, Federal University of Sao Joao del Rei (UFSJ), Central-West Campus, Divinopolis, MG, Brazil
and wide molecular changes in several brain areas [4, 11, 12, 17, 18]. Furthermore, SE leads to temporal lobe epilepsy (TLE), which is characterized by spontaneous recurrent seizures, abnormal synaptic reorganization, mossy fiber sprouting, hippocampal neurodegeneration, and neurogenesis [19–
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