Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ketamine is used widely in emergency departments for a variety of purposes, including procedural sedation and pain management. A major benefit of using ketamine is the rapid onset and lack of respiratory depression. The known side effects include emergence reactions, hallucinations, hypertension, dizziness, nausea, and vomiting. Recent studies have shown the benefit of ketamine for refractory status epilepticus; however, this application of the drug is still being studied. We present a case where ketamine likely induced a seizure in a patient on whom it was used as a single agent in procedural sedation. Seizure is not a known side effect of ketamine in patients without a seizure history. Given the eagerness over additional uses for ketamine, this novel case of a seizure following procedural sedation with ketamine should be of interest to emergency providers.
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PMID:Ketamine Implicated in New Onset Seizure. 3176 99

ATP is a (co)transmitter and signaling molecule in the CNS. It acts at a multitude of ligand-gated cationic channels termed P2X to induce rapid depolarization of the cell membrane. Within this receptor-channel family, the P2X7 receptor (R) allows the transmembrane fluxes of Na+, Ca2+, and K+, but also allows the slow permeation of larger organic molecules. This is supposed to cause necrosis by excessive Ca2+ influx, as well as depletion of intracellular ions and metabolites. Cell death may also occur by apoptosis due to the activation of the caspase enzymatic cascade. Because P2X7Rs are localized in the CNS preferentially on microglia, but also at a lower density on neuroglia (astrocytes, oligodendrocytes) the stimulation of this receptor leads to the release of neurodegeneration-inducing bioactive molecules such as pro-inflammatory cytokines, chemokines, proteases, reactive oxygen and nitrogen molecules, and the excitotoxic glutamate/ATP. Various neurodegenerative reactions of the brain/spinal cord following acute harmful events (mechanical CNS damage, ischemia, status epilepticus) or chronic neurodegenerative diseases (neuropathic pain, Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis) lead to a massive release of ATP via the leaky plasma membrane of neural tissue. This causes cellular damage superimposed on the original consequences of neurodegeneration. Hence, blood-brain-barrier permeable pharmacological antagonists of P2X7Rs with excellent bioavailability are possible therapeutic agents for these diseases. The aim of this review article is to summarize our present state of knowledge on the involvement of P2X7R-mediated events in neurodegenerative illnesses endangering especially the life quality and duration of the aged human population.
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PMID:P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases. 3282 23

The high-fat, low-carbohydrate ketogenic diet (KD) is an established treatment for drug-resistant epilepsy with a proven efficacy. The KD is being explored for Febrile Infection-Related Epilepsy Syndrome (FIRES) and epileptic encephalopathies. There is growing evidence that KD works by targeting dysregulated adaptive and innate immunity that occurs in drug-resistant epilepsy and in refractory status epilepticus. Beyond epilepsy, there are yet additional potential uses in neurological disorders because KD appears to have the broad anti-inflammatory and neuroprotective properties. The KD exerts anti-inflammatory action against a variety of experimental models of neurological disorders including multiple sclerosis, Parkinson's disease, pain, and spinal cord injury. Anti-inflammatory action of KD appears to be mediated by multiple mechanisms. Ketones bodies, caloric restriction, polyunsaturated fatty acids and gut microbiota modifications might be involved in the modulation of inflammation by the KD.
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PMID:Ketogenic diet and Neuroinflammation. 3298 44


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