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For many years, placebos have been conceptualized by their inert content and their use as controls in clinical trials and treatments in clinical practice. Recent research demonstrates that placebo effects are genuine psychobiological phenomenon attributable to the overall therapeutic context, and that placebo effects can be robust in both laboratory and clinical settings. Evidence has …
Continue reading "Placebo Effects: Biological, Clinical and Ethical Advances"
Most of us only go to the doctor when we're not feeling well. You read old magazines in the waiting room, pony up your insurance company's co-pay, answer a stream of seemingly endless questions, and put up with being poked and prodded. And for enduring all of this, you expect something in return. More often than …
Let's say that you stub your toe. Nerves in the toe known as nociceptors, tasked with sensing pain, go into action. They send messages to the spinal cord that pain has occurred; the worse the stub, the more rapidly and powerfully they fire. The spinal cord then releases neurotransmitters to the brain's thalamus, communicating with the …
This article provides an overview of the physiological mechanisms of pain and the important pain pathways. We will discuss pain receptors, transmission of pain signals to the spinal cord and pain pathways within the spinal cord. We will also look at how pain can be modulated at different levels along the pathway. Finally we discuss different types of pain including visceral and neuropathic pain.
There are two main classifications of pain: the commonsensical sort that arises from damaged tissue (nociceptive pain), and the more exotic kind that comes from damage to the system that reports and interprets damage, the nervous system (neuropathic pain). This is the difference between engine trouble and trouble with that light on your dashboard that claims there’s engine trouble. Oddly, there is still no official …
The vast amount of research over the past decades has significantly added to our knowledge of phantom limb pain. Multiple factors including site of amputation or presence of pre-amputation pain have been found to have a positive correlation with the development of phantom limb pain. The paradigms of proposed mechanisms have shifted over the past years from the psychogenic theory to peripheral and central neural changes involving cortical reorganization. More recently, the role of mirror neurons in the brain has been proposed in the generation of phantom pain. A wide variety of treatment approaches have been employed, but mechanism-based specific treatment guidelines are yet to evolve. Phantom limb pain is considered a neuropathic pain, and most treatment recommendations are based on recommendations for neuropathic pain syndromes. Mirror therapy, a relatively recently proposed therapy for phantom limb pain, has mixed results in randomized controlled trials. Most successful treatment outcomes include multidisciplinary measures. This paper attempts to review and summarize recent research relative to the proposed mechanisms of and treatments for phantom limb pain.
Akin to other physiological responses, immune functions can be modified in humans through associative conditioning procedures as part of a learned placebo response. However, it is unclear whether learned immune responses can be produced in patient populations already receiving an immunosuppressive regimen. In the present study, we demonstrate in renal transplant patients who were already receiving immunosuppressive treatment that learned immunosuppressive placebo responses increased efficacy of immunosuppressive medication. These data demonstrate that behavioral conditioning of drug responses may be a promising tool that could be used as a placebo-based dose-reduction strategy in an ongoing immunopharmacological regimen, the aim being to limit unwanted drug adverse effects and to improve treatment efficacy.
The dominant theories of human placebo effects rely on a notion that consciously perceptible cues, such as verbal information or distinct stimuli in classical conditioning, provide signals that activate placebo effects. However, growing evidence suggest that behavior can be triggered by stimuli presented outside of conscious awareness. Here, we performed two experiments in which the responses to thermal pain stimuli were assessed. The first experiment assessed whether a conditioning paradigm, using clearly visible cues for high and low pain, could induce placebo and nocebo responses. The second experiment, in a separate group of subjects, assessed whether conditioned placebo and nocebo responses could be triggered in response to nonconscious (masked) exposures to the same cues. A total of 40 healthy volunteers (24 female, mean age 23 y) were investigated in a laboratory setting. Participants rated each pain stimulus on a numeric response scale, ranging from 0 = no pain to 100 = worst imaginable pain. Significant placebo and nocebo effects were found in both experiment 1 (using clearly visible stimuli) and experiment 2 (using nonconscious stimuli), indicating that the mechanisms responsible for placebo and nocebo effects can operate without conscious awareness of the triggering cues. This is a unique experimental verification of the influence of nonconscious conditioned stimuli on placebo/ nocebo effects and the results challenge the exclusive role of awareness and conscious cognitions in placebo responses.
Placebo effects illustrate the power of the human brain; simply expecting an improvement can alter pain processing and produce analgesia. We induced placebo improvement of both negative and positive feelings (painful and pleasant touch) in healthy humans, and compared the brain processing using functional MRI. Pain reduction dampened sensory processing in the brain, whereas increased touch pleasantness increased sensory processing. Neurocircuitry associated with emotion and reward underpinned improvement of both pain and pleasant touch. Our findings suggest that expectation of improvement can recruit common neurocircuitry, which up- or down-regulates sensory processing, depending on whether the starting point is painful or pleasant. These results promote widening the scope of medical research to improvement of positive experiences and pleasure.
Placebo-induced expectancies have been shown to decrease pain in a manner reversible by opioid antagonists, but little is known about the central brain mechanisms of opioid release during placebo treatment. This study examined placebo effects in pain by using positron-emission tomography with [11C]carfentanil, which measures regional μ-opioid receptor availability in vivo. Noxious thermal stimulation was applied at the same temperature for placebo and control conditions. Placebo treatment affected endogenous opioid activity in a number of predicted μ-opioid receptor-rich regions that play central roles in pain and affect, including periaqueductal gray and nearby dorsal raphe and nucleus cuneiformis, amygdala, orbitofrontal cortex, insula, rostral anterior cingulate, and lateral prefrontal cortex. These regions appeared to be subdivided into two sets, one showing placebo-induced opioid activation specific to noxious heat and the other showing placebo-induced opioid reduction during warm stimulation in anticipation of pain. These findings suggest that a mechanism of placebo analgesia is the potentiation of endogenous opioid responses to noxious stimuli. Opioid activity in many of these regions was correlated with placebo effects in reported pain. Connectivity analyses on individual differences in endogenous opioid system activity revealed that placebo treatment increased functional connectivity between the periaqueductal gray and rostral anterior cingulate, as hypothesized a priori, and also increased connectivity among a number of limbic and prefrontal regions, suggesting increased functional integration of opioid responses. Overall, the results suggest that endogenous opioid release in core affective brain regions is an integral part of the mechanism whereby expectancies regulate affective and nociceptive circuits.