Complex regional pain syndrome (CRPS), a type of primary chronic pain, occurs following trauma or systemic disease and typically affects the limbs. CRPS-induced pain responses result in vascular, cutaneous, and autonomic nerve alterations, seriously impacting the quality of life of affected individuals. We previously identified the involvement of keratinocyte N-methyl-d-asparagic acid (NMDA) receptor subunit 2 B (NR2B) in both peripheral and central sensitizations in CRPS, although the mechanisms whereby NR2B functions following activation remain unclear. Using an in vivo male rat model of chronic post-ischemia pain (CPIP) and an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) cell model, we discovered that oxidative injury occurs in rat keratinocytes and HaCaT cells, resulting in reduced cell viability, mitochondrial damage, oxidative damage of nucleotides, and increased apoptosis. In HaCaT cells, OGD/R induced increases in intracellular reactive oxygen species levels and disrupted the balance between oxidation and antioxidation by regulating a series of antioxidant genes. The activation of NMDA receptors via NMDA exacerbated these changes, whereas the inhibition of the NR2B subunit alleviated them. Co-administration of ifenprodil (an NR2B antagonist) and NMDA (an NMDA receptor agonist) during the reoxygenation stage did not result in any significant alterations. Furthermore, intraplantar injection of ifenprodil effectively reversed the altered gene expression that was observed in male CPIP rats, thereby revealing the potential mechanisms underlying the therapeutic effects of peripheral ifenprodil administration in CRPS. Collectively, our findings indicate that keratinocytes undergo oxidative injury in CRPS, with NMDA receptors playing regulatory roles.

Neurological status is essential and often challenging for neurosurgical residents and also for neurosurgeons to determine surgical management. Pain as a component of the Glasgow Coma Scale (GCS) can be used as a tool in patients, especially an unconscious or comatose patient. In order to elicit this adequate noxious stimulus, a certain amount of pressure-pain threshold is required upon performing either as the central or peripheral technique. The scientific explanation behind each technique is required and needs to be well understood to aid the localisation of the defect in the neurological system. This paper will briefly review the aid of pain as a neurological guide in GCS status assessment.

Long noncoding RNA (lncRNA) is implicated in both cancer development and pain process. However, the role of lncRNA in the development of cancer-induced bone pain (CIBP) is unclear. LncRNA NONRATT014888.2 is highly expressed in tibia related dorsal root ganglions (DRGs) in CIBP rats which function is unknown. CIBP was induced by injection of Walker 256 mammary gland tumor cells into the tibia canal of female SD rats. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) of rats were measured. Down-regulation of NONRATT014888.2 by siRNA in CIBP rats markedly attenuated hind-paw mechanical pain hypersensitivity. LncRNA-predicted target mRNAs analysis and mRNA sequencing results cued Socs3, Npr3 were related with NONRATT014888.2. Intrathecal injection of NONRATT014888.2-siR206 upregulated Npr3 both in mRNA and protein level. Npr3 was co-expressed in NONRATT014888.2-positive DRGs neurons and mainly located in cytoplasm, but not in Glial fibrillary acidic protein (GFAP)-positive cells. Intrathecal injection of ADV-Npr3 upregulated Npr3 expression and enhanced the PWT of CIBP rats. Our results suggest that upregulated lncRNA NONRATT014888.2 contributed to hyperalgesia in CIBP rats, and the mechanism may through downregulation of Npr3.

OBJECTIVE: The goal of this study was to compare our institution\'s recently implemented enhanced recovery after surgery (ERAS) protocol to previous post-operative management for adolescent idiopathic scoliosis patients undergoing posterior spinal fusion, specifically assessing length of stay, opioid consumption, and pain scores.
METHODS: This is a retrospective analysis that compares the length of stay, opioid consumption, and pain scores of patients undergoing posterior spinal fusion for adolescent idiopathic scoliosis. Patients were analyzed prior to the implementation of our ERAS protocol, deemed the traditional pain pathway (TPP), to those who underwent the ERAS pathway. All patients undergoing posterior spinal fusion for adolescent idiopathic scoliosis were included. Patients were excluded if they weighed less than 40kg, had significant comorbidities, or had non-idiopathic causes of scoliosis.
RESULTS: We examined 22 patients in the TPP cohort and 20 in the ERAS cohort. Length of stay in the ERAS cohort was significantly reduced compared to the TPP by 1.7 days (P<0.01). Overall opioid consumption was also significantly reduced in the ERAS with 1.4 ± 0.7 morphine equivalents (ME)/kg compared to the TPP 2.4 ± 1.1 ME/kg (P < 0.01). We found no difference in pain scores between the two groups.
CONCLUSIONS: Implementation of an ERAS pathway at our institution significantly reduced length of stay and opioid consumption in adolescent idiopathic scoliosis patients undergoing posterior spinal fusion. These outcomes reduce morbidity and costs associated with posterior spinal fusion and provide an overall improvement in the quality of care for our patients.

Astrocytes, once thought to be passive cells merely filling the space between neurons in the nervous system, are receiving attention as active modulators of the brain and spinal cord physiology by providing nutrients, maintaining homeostasis, and modulating synaptic transmission. Accumulating evidence indicates that astrocytes are critically involved in chronic pain regulation. Injury induces astrocytes to become reactive, and recent studies suggest that reactive astrocytes can have either neuroprotective or neurodegenerative effects. While the exact mechanisms underlying the transition from resting astrocytes to reactive astrocytes remain unknown, astrocytic calcium increase, coordinated by inflammatory molecules, has been suggested to trigger this transition. In this mini review article, we will discuss the roles of astrocytic calcium, channels contributing to calcium dynamics in astrocytes, astrocyte activations along the pain pathway, and possible relationships between astrocytic calcium dynamics and chronic pain.

Dhamma, which Lord Buddha has presented to people after his enlightenment, analyzes every phenomenon and objects into their ultimate elements. The explanation of sensory system is also found in a part of Dhamma named Abhidhammapitaka, the Book of the Higher Doctrine in Buddhism. To find out the relationship between explanation of pain in the present neuroscience and the explanation of pain in Abhidhamma, the study was carried out by the use of a comprehensive review. The comparisons were in terms of peripheral stimulation, signal transmission, modulation, perception, suffering, determination and decision making for the responding to pain. We found that details of the explanation on pain mechanism and perception in Abhidhamma could associate well with our present scientific knowledge. Furthermore, more refinement information about the process and its function in particular aspects of pain perception were provided in Abhidhammapitaka.

The pathophysiology of pain is a complex process that varies according to duration (eg, acute, chronic) or type (eg, nociceptive, neuropathic, psychogenic). Perioperative nurses should understand the pathways that lead to pain to better assist in managing patients\' pain symptoms. Approaching pain from a patient-centered stance includes acknowledging that pain is defined entirely by the subjective experience of the patient, which may not be proportional with the level of tissue damage. This article provides a brief description of the pathophysiology of pain and the components of nociceptive and neuropathic pain pathways to aid the perioperative nurse in pain management.

Studies have reported divergent behavioral effects of depression on spontaneous vs. stimulus-evoked pain. However, the underlying neurobiological mechanisms are still unclear. The present study used a depression model of unpredictable chronic mild stress (UCMS) and pain models for spontaneous pain (i.e., the formalin test) and acute evoked pain (i.e., noxious thermal stimulation) in rats. The activity of neurons within thalamo-cortical circuits in the lateral and medial pain pathways was recorded by a multiple-channel recording technique, and behaviors were observed simultaneously. The results confirmed our previous findings that rats exposed to UCMS tended to exhibit decreased pain sensitivity to experimental stimuli but increased behavioral responses to ongoing pain. Based on the analysis of single-unit responses, the results demonstrated that the processing of spontaneous vs. evoked pain in a depressive-like state was altered in the opposite direction (activation vs. inhibition). The ensemble encoding analysis revealed that exposure to UCMS gave rise to enhanced inter-regional functional connectivity in spontaneous pain processing, but did not influence that of evoked pain. In addition, different brain activation patterns underlying the processing of spontaneous vs. evoked pain were observed. These findings revealed that the distinct response patterns of neurons within the pain-related brain circuits, especially in the affective pain pathway, mediate the divergent effects of depression on spontaneous vs. evoked pain. This is also the first report on the electrophysiology of depression models that provides direct evidence that the effect of depression on spontaneous and evoked pain may involve different brain mechanisms.