In 2005, the first direct evidence of opioid-mediated placebo analgesia was published (Zubieta et al., 2005). In vivo receptor-binding techniques using the radiotracer carfentanil, a µ-opioid agonist, were used to show that a placebo procedure activates µ-opioid neurotransmission in the dorsolateral prefrontal cortex, the anterior cingulate cortex, the insula, and the nucleus accumbens (Fig. 4.7). …
Placebo effects can be very effective in certain pain conditions, but their use is still highly controversial. Several studies show that patients would accept a placebo treatment under certain circumstances, particularly when they are informed prior to the treatment or when there are no effective treatment alternatives. This study examines the question, which factors influence the degree of acceptability of a hypothetical placebo application.
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.
Persistent or chronic pain is the primary reason people seek medical care, yet current therapies are either inadequate for certain types of pain or cause intolerable side effects. Recently, pain neurobiologists have identified a number of cellular and molecular processes that lead to the initiation and maintenance of pain. Understanding these underlying mechanisms has given significant promise for the development of more effective, more specific pain therapies in the near future.
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.