Chronic pain is one of the most disabling medical conditions globally, yet, to date, we lack a satisfying theoretical framework for research and clinical practice. Over the prior decades, several frameworks have been presented with biopsychosocial models as the most promising. However, in translation to clinical practice, these models are often applied in an overly reductionist manner, leaving much to be desired. In particular, they often fail to characterize the complexities and dynamics of the lived experience of chronic pain. Recently, (...) an enactive, affordance-based approach has been proposed, opening up new ways to view chronic pain. This model characterizes how the persistence of pain alters a person’s field of affordances: the unfolding set of action possibilities that a person perceives as available to them. The affordance-based model provides a promising perspective on chronic pain as it allows for a systematic investigation of the interactive relation between patients and their environment, including characteristic alterations in the experience of their bodies and the space they inhabit. To help bridge the gap from philosophy to clinical practice, we unpack in this paper the core concepts of an affordance-based approach to chronic pain and their clinical implications, highlighting aspects that have so far received insufficient attention. We do so with an analogy to playing video games, as we consider such comparative illustration a useful tool to convey the complex concepts in an affordance-based model and further explore central aspects of the lived experience of chronic pain. (shrink)

Raja Rammohun Roy.--Maharshi Devendranath Tagore.--Keshab Chandra Sen.--Paramahansadeva Ramakrishna.--Swami Vivekananda.--Swami Dayananda.--Radindranath.--Gandhi.--Sri Aurobindo.

Aim Genetic research representative of the population is crucial to understanding the underlying causes of many diseases. In a prospective evaluation of informed consent we assessed the willingness of individuals of different ethnicities, gender and drug dependence history to participate in genetic studies in which their genetic sample could be shared with a repository at the National Institutes of Health. Methods Potential subjects were recruited from the general population through the use of flyers and referrals from previous participants and clinicians (...) with knowledge of our study. They could consent to 11 separate choices so that they could specify how and with whom their genetic sample could be shared. Rates of affirmative consent were then analysed by gender, ethnicity and drug dependence history. Results Of 1416 volunteers enrolled, 99.7% gave affirmative informed consent for studies of addiction conducted in our laboratory. No significant difference was found for participation in genetic studies conducted in our laboratory by gender, ethnicity or drug dependence history. Over all 11 questions, individuals with a history of drug use were more likely to agree to consent to participate in our study than were healthy volunteers. Conclusion A high percentage of each category of gender, ethnicity and drug history, gave affirmative consent at all levels. The level of detail in and the amount of time spent reviewing the informed consent, and a relationship of trust with the clinical investigator may contribute to this outcome. (shrink)

The present review highlights an association between autism, Alzheimer disease , and fragile X syndrome . We propose a conceptual framework involving the amyloid-beta peptide , Abeta precursor protein , and fragile X mental retardation protein based on experimental evidence. The anabolic effect of the secreted alpha form of the amyloid-beta precursor protein may contribute to the state of brain overgrowth implicated in autism and FXS. Our previous report demonstrated that higher plasma sAPPalpha levels associate with more severe symptoms of (...) autism, including aggression. This molecular effect could contribute to intellectual disability due to repression of cell-cell adhesion, promotion of dense, long, thin dendritic spines, and the potential for disorganized brain structure as a result of disrupted neurogenesis and migration. At the molecular level, APP and FMRP are linked via the metabotropic glutamate receptor 5 . Specifically, mGluR5 activation releases FMRP repression of APP mRNA translation and stimulates sAPP secretion. The relatively lower sAPPalpha level in AD may contribute to AD symptoms that significantly contrast with those of FXS and autism. Low sAPPalpha and production of insoluble Abeta would favor a degenerative process, with the brain atrophy seen in AD. Treatment with mGluR antagonists may help repress APP mRNA translation and reduce secretion of sAPP in FXS and perhaps autism. (shrink)