In this research, meta-analyses were performed to evaluate associations between primary appraisals of pain as a source of threat and/or challenge and responses to 1) noxious laboratory stimuli and 2) chronic noncancer pain. Twenty-two laboratory pain studies comprising 2,031 participants and 59 chronic pain studies based on 9,135 patients were identified for analysis. For laboratory pain, elevated threat appraisals were linked to overall increases in reported pain, reduced pain tolerance, and high levels of passive coping. Method of measuring appraisal as well as type and duration of noxious stimulation moderated some of these associations. Challenge appraisals were related to more pain tolerance and less passive coping but not pain intensity. For chronic pain studies, threat appraisals had positive overall correlations with pain intensity, impairment, affective distress, and passive coping but were negatively related to active coping. The pattern of associations between challenge appraisals and outcomes was largely complementary. Appraisal scale used and gender were consistent moderators of appraisal-outcome relations in chronic pain samples. In sum, appraisals of pain as a source of potential damage or opportunity have robust associations with responses to acute laboratory pain and ongoing chronic pain.

Chronic pain is pain that persists beyond the expected period of healing. The subjective experience of chronic pain results from pathological brain network interactions, rather than from persisting physiological sensory input of nociceptors. We hypothesize that pain is an imbalance between pain evoking dorsal anterior cingulate cortex and somatosensory cortex and pain suppression (i.e. pregenual anterior cingulate cortex). This imbalance can be measured objectively by current density ratios between pain input and pain inhibition. A balance between areas involved in pain input and pain suppression requires communication, which can be objectively identified by connectivity measures, both functional and effective connectivity. In patients with chronic neuropathic pain, electroencephalography is performed with source localization demonstrating that pain is reflected by an abnormal ratio between the dorsal anterior cingulate cortex, somatosensory cortex and pregenual anterior cingulate cortex. Functional connectivity demonstrates decreased communication between these areas, and effective connectivity puts the culprit at the dorsal anterior cingulate cortex, suggesting that the problem is related to abnormal behavioral relevance attached to the pain. In conclusion, chronic pain can be considered as an imbalance between pain input and pain suppression.

Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mice and humans. We examined the role of Nav1.7 as well as Nav1.3, Nav1.8, and Nav1.9 in different mouse models of chronic pain. Constriction-injury-dependent neuropathic pain is abolished when Nav1.7 is deleted in sensory neurons, unlike nerve-transection-related pain, which requires the deletion of Nav1.7 in sensory and sympathetic neurons for pain relief. Sympathetic sprouting that develops in parallel with nerve-transection pain depends on the presence of Nav1.7 in sympathetic neurons. Mechanical and cold allodynia required distinct sets of neurons and different repertoires of sodium channels depending on the nerve injury model. Surprisingly, pain induced by the chemotherapeutic agent oxaliplatin and cancer-induced bone pain do not require the presence of Nav1.7 sodium channels or Nav1.8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype.

Everyday variations in night sleep in healthy pain-free subjects are at most weakly associated with pain, whereas strong alterations (eg, sleep deprivation, insomnia) lead to hyperalgesic pain changes. Since it remains unclear how substantial sleep alterations need to be in order to affect the pain system and lead to a coupling of both functions, the present study aimed at providing sufficient variance for co-variance analyses by examining a sample consisting of both healthy subjects and chronic pain patients.

Numerous studies demonstrate elevated pain sensitivity and impaired conditioned pain modulation (CPM) in patients with chronic musculoskeletal pain compared to healthy individuals; however, the time course of changes in pain sensitivity and CPM after the development of a chronic pain condition is unclear. Secondary analysis of data from a prospective investigation examined changes in evoked pain sensitivity and CPM before and after development of chronic neck pain (CNP). 171 healthy office workers participated in a baseline assessment, followed by monthly online questionnaires to identify those who developed CNP over the subsequent year. These individuals (N = 17) and a cohort of participants (N = 10) who remained pain-free during the follow-up period returned for a 12-month follow-up assessment of mechanical and thermal pain sensitivity and CPM. Pain sensitivity measures did not differ between groups at baseline; however, cold pain threshold decreased in the CNP group at follow-up (p < 0.05). CPM was lower at baseline in the CNP group compared to those who reported no neck pain (p < 0.02) and remained unchanged one year later. These findings indicate that CPM is reduced in healthy individuals prior to the development of chronic neck pain and the subsequent reduction of thresholds for cold but not pressure pain.

Individuals affected by chronic lower-back pain and obesity have an increased risk of long-lasting disability. In this study, we aimed to explore the contribution of kinesiophobia and pain catastrophizing in explaining pain intensity and pain-related disability in chronic lower-back pain associated to obesity. A cross-sectional study on 106 participants with obesity and chronic lower-back pain was performed. We assessed pain intensity, pain disability, pain catastrophizing, and kinesiophobia levels through self-reporting questionnaire. Hierarchical regressions were performed to assess the role of pain catastrophizing and kinesiophobia on pain intensity and pain disability. According to the results, kinesiophobia, but not pain catastrophing, significantly explained both pain intensity and pain-related disability. Kinesiophobia might play a significant role in enhancing pain-related disability and the pain intensity in individuals with chronic lower-back pain and obesity. We encourage future studies in which beliefs and cognition towards pain might be a therapeutic target in interdisciplinary pain management interventions.

A brief account is first given of the incidence and characteristics of cancer pain. The management of such pain should involve treatment of the malignant condition, psychological support, pharmacological supplementation and interruption of the pain pathways. The paper proceeds to detail the various methods by which this last objective can be achieved. The most widely applicable method is intrathecal injection of a neurolytic agent-phenol, chlorocresol or alcohol. This will provide 2-4 months relief in about 60 per cent patients. More prolonged and extensive relief can be done by cordotomy; the percutaneous procedure has the advantages of involving no general anaesthesia and only brief hospitalisation. For patients with hormone dependent tumours and those with widespread pain, relief can be obtained by destruction of the pituitary gland with absolute alcohol. The injection is carried out through a needle inserted into the gland via the nose and sphenoid sinus; one or two repeat injections may be necessary. When pain is partly due to involvement of autonomic nerves, it is necessary to carry out appropriate autonomic neurolysis, e.g. coeliac plexus block for visceral pain. Finally, the paper deals with non-invasive pain relief techniques, especially dorsal column and central nerve stimulation.

Clinical experience teaches us that patients are willing to accept postoperative pain, despite high pain intensity scores. Nevertheless, relationships between pain scores and other methods of pain assessment, e.g. acceptability of pain or its interference with physical functioning, are not fully established. Our aims were to examine these relationships.

Understanding the molecular mechanisms associated with disease is a central goal of modern medical research. As such, many thousands of experiments have been published that detail individual molecular events that contribute to a disease. Here we use a semi-automated text mining approach to accurately and exhaustively curate the primary literature for chronic pain states. In so doing, we create a comprehensive network of 1,002 contextualized protein-protein interactions (PPIs) specifically associated with pain. The PPIs form a highly interconnected and coherent structure, and the resulting network provides an alternative to those derived from connecting genes associated with pain using interactions that have not been shown to occur in a painful state. We exploit the contextual data associated with our interactions to analyse subnetworks specific to inflammatory and neuropathic pain, and to various anatomical regions. Here, we identify potential targets for further study and several drug-repurposing opportunities. Finally, the network provides a framework for the interpretation of new data within the field of pain.

There is an ongoing debate whether the neuropeptide oxytocin (OT) modulates pain processing in humans. This study differentiates behavioral and neuronal OT effects on pain perception and pain anticipation by using a Pavlovian conditioning paradigm. Forty-six males received intranasally administered OT in a randomized, double-blind, placebo-controlled group design. Although OT exerted no direct effect on perceived pain, OT was found to modulate the blood oxygen level-dependent response in the ventral striatum for painful versus warm unconditioned stimuli and to decrease activity in the anterior insula (IS) with repeated thermal pain stimuli. Regarding pain anticipation, OT increased responses to CSpain versus CSminus in the nucleus accumbens. Furthermore, in the OT condition increased correct expectations, particularly for the most certain conditioned stimuli (CS)-unconditioned stimuli associations (CSminus and CSpain) were found, as well as greatest deactivations in the right posterior IS in response to the least certain condition (CSwarm) with posterior IS activity and correct expectancies being positively correlated. In conclusion, OT seems to have both a direct effect on pain processing via the ventral striatum and by inducing habituation in the anterior IS as well as on pain anticipation by boostering associative learning in general and the neuronal conditioned fear of pain response in particular. PERSPECTIVE: The neuropeptide OT has recently raised the hope to offer a novel avenue for modulating pain experience. This study found OT to modulate pain processing and to facilitate the anticipation of pain, inspiring further research on OT effects on the affective dimension of the pain experience.

This topical review presents the current challenges in defining chronic pain in infants, summarizes evidence from animal and human infant studies regarding the biological processes necessary for chronic pain signaling, and presents observational/experiential evidence from clinical experts. A literature search of four databases (CINAHL, EMBASE, PsycINFO, and MEDLINE) was conducted, along with hand searches of reference lists. Evidence from animal studies suggest that important neurophysiological mechanisms, such as the availability of key neurotransmitters needed for maintenance of chronic pain, may be immature or absent in the developing neonate. In some cases, human infants may be significantly less likely to develop chronic pain. However, evidence also points to altered pain perception, such as allodynia and hyperalgesia, with significant injury. Moreover, clinicians and parents in pediatric intensive care settings describe groups of infants with altered behavioral responses to repeated or prolonged painful stimuli, yet agreement on a working definition of chronic pain in infancy remains elusive. While our understanding of infant chronic pain is still in the rudimentary stages, a promising avenue for the future assessment of chronic pain in infancy would be to develop a clinical tool that uses both neurophysiological approaches and clinical perceptions already presented in the literature.

BACKGROUND Pain prevalence has been investigation in many developed countries, but integrated information about pain prevalence in Chinese hospitals is lacking. To achieve better pain treatment of hospitalized patients, pain management needs to be investigated. The present descriptive and cross-sectional study was performed to demonstrate the prevalence of pain by comparison with the 4 traditional vital signs, and to investigate pain management in a Chinese teaching hospital. MATERIAL AND METHODS Structured and systematic interviews were undertaken by independent researchers. During a patient's hospitalization, the prevalence of pain and the 4 vital signs were recorded. Then, the catalog, severity, causes, duration of pain, and pain management were assessed. RESULTS We found: (1) 63.36% of patients (3248 in total) suffered from pain while in hospital, which was 1.8~2.8 times higher than the prevalence of abnormality of the 4 vital signs. (2) 76% of patients had moderate pain and 21.98% had severe pain. (3) Pain intensity differed among patients with different diseases, but did not differ by demographic factors. (4) Acute and chronic pain were present in 68% and 26% of patients, respectively. In addition, 16% of the patients had neuropathic pain. (5) More than half of the patients with pain refused to receive pain-relief medication because they worried about addiction to opioids and the adverse effects of analgesics. (6) Most medical staff properly understood the 3 ladder analgesics. CONCLUSIONS The prevalence of pain is higher than the abnormality of the 4 traditional vital signs in a Chinese hospital. Although pain management has broadly improved, more patient education is necessary.

Pain is a prevalent symptom in patients with advanced cancer. Recognition of prognostic factors associated with pain intensity, could help provide better assessment, leading to better pain management.

Offset analgesia (OA) and conditioned pain modulation (CPM) are frequently used paradigms to assess the descending pain modulation system. Recently, it was shown that both paradigms are reduced in chronic pain, but the influence of acute pain has not yet been adequately examined.

Pain neurophysiology education (PNE) is an educational intervention for patients with chronic pain. PNE purports to assist patients to reconceptualise their pain away from the biomedical model towards a more biopsychosocial understanding by explaining pain biology. This study aimed to explore the extent, and nature, of patients' reconceptualisation of their chronic low back pain (CLBP) following PNE. Eleven adults with CLBP underwent semistructured interviews before and three weeks after receiving PNE. Interviews were transcribed verbatim and thematically analysed in a framework approach using four a priori themes identified from our previous research: (1) degrees of reconceptualisation, (2) personal relevance, (3) importance of prior beliefs, and (4) perceived benefit of PNE. We observed varying degrees of reconceptualisation from zero to almost complete, with most participants showing partial reconceptualisation. Personal relevance of the information to participants and their prior beliefs were associated with the degree of benefit they perceived from PNE. Where benefits were found, they manifested as improved understanding, coping, and function. Findings map closely to our previous studies in more disparate chronic pain groups. The phenomenon of reconceptualisation is applicable to CLBP and the sufficiency of the themes from our previous studies increases confidence in the certainty of the findings.

Pain drawings (PDs) are an important tool to evaluate, communicate, and objectify pain. In the past few years, there has been a shift toward tablet-based acquisition of PDs, and several studies have been conducted to test the usefulness, reliability, and repeatability of electronic PDs. However, to our knowledge, no study has investigated the potential role of electronic PDs in the clinical assessment and treatment of inpatients in acute pain situations.

Neuropathic pain causes patients feel indescribable pain. Deep Brain Stimulation (DBS) is one of the treatment methods in neuropathic pain but the action mechanism is still unclear. To study the effect and mechanism of analgesic effects from DBS in neuropathic pain and to enhance the analgesic effect of DBS, we stimulated the ventral posterolateral nucleus (VPL) in rats.

Our central research question was, in England, are geographical inequalities in opioid use driven by health need (pain)? To answer this question, our study examined: (1) if there are regional inequalities in rates of chronic pain prevalence, pain intensity and opioid utilisation in England; (2) if opioid use and chronic pain are associated after adjusting for individual-level and area-level confounders.

When in pain, pain relief is much sought after, particularly for individuals with chronic pain. In analogy to augmentation of the hedonic experience ("liking") of a reward by the motivation to obtain a reward ("wanting"), the seeking of pain relief in a motivated state might increase the experience of pain relief when obtained. We tested this hypothesis in a psychophysical experiment in healthy human subjects, by assessing potential pain-inhibitory effects of pain relief "won" in a wheel of fortune game compared with pain relief without winning, exploiting the fact that the mere chance of winning induces a motivated state. The results show pain-inhibitory effects of pain relief obtained by winning in behaviorally assessed pain perception and ratings of pain intensity. Further, the higher participants scored on the personality trait novelty seeking, the more pain inhibition was induced. These results provide evidence that pain relief, when obtained in a motivated state, engages endogenous pain-inhibitory systems beyond the pain reduction that underlies the relief in the first place. Consequently, such pain relief might be used to improve behavioral pain therapy, inducing a positive, perhaps self-amplifying feedback loop of reduced pain and improved functionality.

Pain disrupts the daily and social lives of patients with neuropathic pain. Effective treatment of neuropathic pain is difficult. Pharmacological treatments for neuropathic pain are limited, and 40-60% of patients do not achieve even partial relief of their pain. This study created a chronic constriction injury (CCI) model in rats to examine the effects of regular exercise on neuropathic pain relief, elucidate the mechanism, and determine the effects of neuropathic pain in the hippocampus.