Pain
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Chronic pain is common among children and adolescents; however, the diagnoses in the newly developed 11th revision of the International Classification of Diseases (ICD-11) chronic pain chapter are based on adult criteria, overlooking pediatric neurodevelopmental differences. The chronic pain diagnoses have demonstrated good clinical applicability in adults, but to date, no field study has examined these diagnoses to the most specific diagnostic level in a pediatric sample. The current study aimed to explore pediatric representation within the ICD-11, with focus on chronic primary pain. ⋯ The latter also exhibited the lowest agreement between HCPs and algorithm. The current study underscores the need for evidence-based improvements to the ICD-11 diagnostic criteria in pediatrics. Developing pediatric coding notes could improve the visibility of patients internationally and improve the likelihood of receiving reimbursement for necessary treatments through accurate coding.
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Spinal cord stimulation (SCS) is an effective modality for pain treatment, yet its underlying mechanisms remain elusive. Neurokinin 1 receptor-positive (NK1R + ) neurons in spinal lamina I play a pivotal role in pain transmission. To enhance our mechanistic understanding of SCS-induced analgesia, we investigated how different SCS paradigms modulate the activation of NK1R + neurons, by developing NK1R-Cre;GCaMP6s transgenic mice and using in vivo calcium imaging of superficial NK1R + neurons under anesthesia (1.5% isoflurane). ⋯ However, at low intensity (20% MoT), the 30-minute 900-Hz SCS only induced persistent neuronal inhibition in naïve mice, but not in SNI-t mice. In conclusion, both 10-minute high-intensity SCS and 30-minute SCS at moderate intensity inhibit the activation of superficial NK1R + neurons, potentially attenuating spinal nociceptive transmission. Furthermore, in vivo calcium imaging of NK1R + neurons provides a new approach for exploring the spinal neuronal mechanisms of pain inhibition by neuromodulation pain therapies.
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Na v 1.9 is of interest to the pain community for a number of reasons, including the human mutations in the gene encoding Na v 1.9, SCN11a , that are associated with both pain and loss of pain phenotypes. However, because much of what we know about the biophysical properties of Na v 1.9 has been learned through the study of rodent sensory neurons, and there is only 76% identity between human and rodent homologs of SCN11a , there is reason to suggest that there may be differences in the biophysical properties of the channels in human and rodent sensory neurons, and consequently, the contribution of these channels to the control of sensory neuron excitability, if not pain. Thus, the purpose of this study was to characterize Na v 1.9 currents in human sensory neurons and compare the properties of these currents with those in rat sensory neurons recorded under identical conditions. ⋯ However, we noted a number of potentially important differences between the currents in human and rat sensory neurons including a lower threshold for activation, higher threshold for inactivation, slower deactivation, and faster recovery from slow inactivation. Human Na v 1.9 was inhibited by inflammatory mediators, whereas rat Na v 1.9 was potentiated. Our results may have implications for the role of Na v 1.9 in sensory, if not nociceptive signaling.