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Introduction: Intraoperative monitoring of nociception has made great progress in adult anesthesia. However, pediatric data are scarce. The Nociception Level (NOL) is one of the most recent indexes of nociception. Its originality is that it provides a multiparametric assessment of nociception. In adults, NOL monitoring allowed lower perioperative opioid requirements, hemodynamic stability, and qualitative postoperative analgesia. So far, the NOL has never been used in children. Our objective was to validate the ability of NOL to provide a quantitative assessment of nociception in anesthetized children.
Methods: In 5-12 years old children anesthetized with sevoflurane and alfentanil (10 µg kg), before surgical incision, we performed three standardized tetanic stimulations (5 s, 100 Hz) of different intensities (10-30-60 mA) in a randomized order. NOL, heart rate, blood pressure and Analgesia-Nociception Index variations were assessed after each stimulation.
Results: Thirty children were included. Data were analyzed with a covariance pattern linear mixed regression model. NOL increased after the stimulations (p < 0.05 at each intensity). NOL response was influenced by stimulation intensity (p < 0.001). Heart rate and blood pressure were barely modified by the stimulations. Analgesia-Nociception Index decreased after the stimulations (p < 0.001 at each intensity). Analgesia-Nociception index response was not influenced by stimulation intensity (p = 0.064). NOL and Analgesia-Nociception Index responses were significantly correlated (Pearson r = 0.47; p < 0.001).
Conclusions: NOL allows a quantitative assessment of nociception under anesthesia in 5-12 years-old children. This study provides a solid basis for all future investigations on NOL monitoring in pediatric anesthesia.
Registration: NCT05233449.
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http://dx.doi.org/10.1016/j.accpm.2023.101207 | DOI Listing |
Brain Res
September 2025
Department of Neurology, Shanghai Sixth People's Hospital, Shanghai 200233, China. Electronic address:
Migraine is a complex neurological disorder influenced by multiple genetic susceptibility factors, yet current animal models fail to fully recapitulate its human-specific pathophysiology. In this study, we explored the potential mechanisms underlying migraine by examining functional abnormalities and molecular dysregulation in glutamatergic neurons derived from induced pluripotent stem cells (iPSCs) of migraine patients. As key excitatory cells in the central nervous system, glutamatergic neurons are implicated in migraine through altered excitability, ion channel dysfunction, and dysregulation of nociceptive signaling molecules.
View Article and Find Full Text PDFPain Rep
October 2025
Physiology, Pharmacology and Neuroscience, School of Life Sciences, The University of Nottingham, Nottingham, United Kingdom.
Introduction: The dorsal horn (DH) of the spinal cord is physiologically immature at birth. Spinal excitability increases and wide dynamic range (WDR) neurons in lamina V have lowered activation thresholds and larger receptive field sizes.
Objective: The DH is composed of 5 laminae containing diverse interneuronal populations yet our understanding of the physiology of the DH is based on behavioural studies or extrapolation of single cell WDR recordings to the whole network.
Eur J Pain
October 2025
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Background: Pain catastrophising is a maladaptive cognitive-emotional trait linked to greater pain severity and poorer outcomes, yet its neurophysiological correlates remain unclear.
Objectives: We tested whether pain catastrophising amplifies cortical responses to nociceptive input, independent of subjective pain intensity.
Methods: Fifty-two healthy adults underwent EEG during painful laser stimulation (n = 29; mean age 24.
The endocannabinoid (eCB) system-comprising cannabinoid receptors, eCBs (anandamide- AEA, 2-arachidonoylglycerol-2-AG) and related -acylethanolamines (NAEs; palmitoylethanolamide-PEA, and oleoylethanolamide-OEA), and metabolizing enzymes (e.g., fatty acid amide hydrolase; FAAH)-modulates nociceptive circuits in rodents.
View Article and Find Full Text PDFNeuron
September 2025
Department of Dermatology, University of Wisconsin-Madison, Madison, WI, USA; Carbone Cancer Center, University of Wisconsin-Madison, Madison, WI, USA; Department of Cell and Regenerative Biology, University of Wisconsin-Madison, Madison, WI, USA. Electronic address:
Peripheral sensory neurons, once regarded merely as a passive route for nociceptive signals, are now acknowledged as active participants in solid tumor progression. This review explores how sensory neurons influence and are influenced by the tumor microenvironment (TME) through both chemical and electrical signaling, underscoring their pivotal role in the emerging field of cancer neuroscience. We summarize recent findings indicating that cancer-neuron interactions vary among different organs and experimental models, highlighting the ways in which various tumors recruit and reprogram sensory neurons to establish mutual communication loops that foster malignancy.
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