Pain
-
The failure to translate research evidence into day-to-day clinical practices is identified as a significant reason for suboptimal quality care across the health system, including procedural pain management in children. Clinical practice guidelines (CPGs) have been developed to assist in this process by synthesizing and interpreting research evidence for end users. Numerous CPGs have been developed for procedural pain management in children, yet gaps persist in the adoption of best practices. ⋯ Specific areas that will be addressed include partnerships with stakeholders, rigor of guideline development, issues of implementation, and editorial independence. The work of HELPinKIDS was guided by a KT map, which identified, at a high level, the target audiences, key messages, tools, and strategies that could be used to communicate, disseminate, and implement the CPG into diverse settings. Examples of impact at both the individual and systems levels from HELPinKIDS KT activities are also presented.
-
Much evidence from pain patients and animal models shows that chronic pain does not exist in a vacuum but has varied comorbidities and far-reaching consequences. Patients with long-term pain often develop anxiety and depression and can manifest changes in cognitive functioning, particularly with working memory. Longitudinal studies in rodent models also show the development of anxiety-like behavior and cognitive changes weeks to months after an injury causing long-term pain. ⋯ Nevertheless, studies in humans reveal that lifestyle choices, such as the practice of meditation or yoga, can reduce pain perception and have the opposite effect on the brain as does chronic pain. In rodent models, studies show that physical activity and a socially enriched environment reduce pain behavior and normalize brain function. Together, these studies suggest that the burden of chronic pain can be reduced by nonpharmacological interventions.
-
Existing analgesics are not efficacious in treating all patients with chronic pain and have harmful side effects when used long term. A deeper understanding of pain signaling and sensitization could lead to the development of more efficacious analgesics. Nociceptor sensitization occurs under conditions of inflammation and nerve injury where diverse chemicals are released and signal through receptors to reduce the activation threshold of ion channels, leading to an overall increase in neuronal excitability. ⋯ Thus, PIP2 sits at a critical convergence point for multiple receptors, ion channels, and signaling pathways that promote and maintain chronic pain. Decreasing the amount of PIP2 in neurons was recently shown to attenuate pronociceptive signaling and could provide a novel approach for treating pain. Here, we review the lipid kinases that are known to regulate pain signaling and sensitization and speculate on which additional lipid kinases might regulate signaling in nociceptive neurons.
-
This review presents a general model for the understanding of pain, placebo, and chronification of pain in the framework of cognitive neuroscience. The concept of a computational cost-function underlying the functional imaging responses to placebo manipulations is put forward and demonstrated to be compatible with the placebo literature including data that demonstrate that placebo responses as seen on the behavioural level may be elicited on all levels of the neuroaxis. In the same vein, chronification of pain is discussed as a consequence of brain mechanisms for learning and expectation. ⋯ Women are greatly overrepresented in patients with chronic pain. Hence, both from a general standpoint and from reasons of health equity, it is of essence to advance research and care efforts. Success in these efforts will only be granted with better theoretical concepts of chronic pain mechanisms that maps into the framework of cognitive neuroscience.
-
Development and application of psychophysical test paradigms to assess endogenous pain modulation in healthy controls and in patients yielded large body of data over the last 2 decades. These tests can assist in predicting pain acquisition, in characterizing pain syndromes and related dysfunctions of pain modulation, and in predicting response to treatment. This chapter reviews the development of thought on pain modulation in the clinical setup, focusing on conditioned pain modulation, and update on accumulated data regarding the mechanism, protocols of administration, and applications in the clinic.