ReviewDrug design, development and therapy2025
Chloral Hydrate's Impact on Brain Development: From Clinical Safety to Molecular Mechanisms.
Review in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Decoding neuroimmune ferroptotic vulnerability in isoflurane-induced neonatal neurotoxicity via the SLC7A11/GPX4 axis.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chloral hydrate remains an irreplaceable first-line sedative in pediatric clinical practice, widely used for outpatient procedures and imaging examinations due to its proven efficacy and unique suitability for children. Despite its clinical indispensability, the impact of chloral hydrate on the developing central nervous system (CNS) in children remains largely unelucidated - a critical knowledge gap, given that children's immature blood-brain barrier (BBB) and high neuronal plasticity render their developing brains more vulnerable to pharmacological agents. Existing evidence demonstrates a significant negative correlation between the duration of chloral hydrate use and pediatric intelligence quotient (PIQ): longer usage is associated with lower PIQ scores. Prolonged use may impair non-verbal abilities reflected in PIQ, thereby compromising overall cognitive function - highlighting a critical clinical safety concern. By synthesizing current clinical observations and molecular mechanisms, this paper proposes that chloral hydrate may disrupt neurodevelopment through pathways including N-methyl-D-aspartate (NMDA) receptors, γ-aminobutyric acid (GABA) receptors, and the Mitogen-Activated Protein Kinase-Extracellular Signal-Regulated Kinase (MEK-ERK) signaling pathway. Basing on these findings, caution should be exercised regarding the use of chloral hydrate - particularly its long-term administration. Long-term follow-up of exposed children is recommended to continuously monitor cognitive function and neurodevelopment, with a focus on non-verbal abilities and overall intellectual development. Future research should prioritize prospective, long-term neurodevelopmental follow-up studies, specifically in children exposed to chloral hydrate, combined with neuroimaging and biomarker studies, to further explore its potential effects on neurodevelopment. In summary, this article synthesizes existing evidence to elucidate the effects of chloral hydrate on the developing brain, spanning clinical observations to underlying molecular mechanisms, with the aim of clarifying its potential implications for pediatric neurodevelopment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.