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The effect of placebo on pain is a relatively new area of study bolstered by findings stating that placebo does reduce pain. By creating an expectation that pain will be relieved, placebo is thought to stimulate the production of endorphins. This is known as placebo analgesia. The study by Wager et al. aims to further support this finding by determining the effects of placebo on parts of the brain which deal with the psychologic (pain modulation) and sensory (pain transmission) aspects of pain, these being the prefrontal cortex and the pain matrix respectively.

Wager’s et al. study was conducted facing controversy involving diverging views. Some believe that placebo modifies the neural transmission of pain; some posit that it is related to pain affect, while others say that findings were biased in favor of the researchers’ claims. Wager et al. propose that if placebo truly relieves pain, then it should produce the predictable physiologic responses in the brain associated with pain modulation and transmission. It is significant in that it takes a more direct approach in clarifying the debate regarding the mechanism of placebo analgesia.     

Literature provides indirect evidence that placebo relieves pain basing on the fact that analgesic effects are diminished with the use of opioid antagonists such as Narcan suggesting that placebo utilizes the opioid mechanism. Prior studies then highly recommend the use of neuro-imaging because, unlike pain medicine, placebo cannot be studied with respect to its active components, metabolism, and absorption at the cellular level. The use of neuro-imaging provides the most straightforward method of inferring how pain processing actually occurs.

The study used an experimental approach involving two separate experiments using fMRI technology with 23 to 24 human participants. The first experiment was performed to validate that the pain matrix and the prefrontal area do respond to pain stimuli evidenced by changes in activity levels and as such should respond to placebo. In the second experiment, different levels of different types of pain were administered followed by placebo; the participants were asked to rate their pain. The ratings were then correlated with brain activities in the pain matrix and prefrontal areas shown in the fMRI images.

In brief, the results show that placebo resulted in activity decline in the pain matrix concerned with pain transmission and is consistent with the participants’ reports of pain relief. Additionally, placebo analgesia occurred along with the increased prefrontal cortex or pain modulation activity. Both findings imply that placebo analgesia is the outcome of both psychologic and sensory processes, not just one. It further provides evidence that placebo effect is not the product of researcher bias but can, in fact, be measured. The conclusions were well supported by quantitative data and correlation involving participant rating of pain relief, post pain stimuli and subsequent placebo use, and brain activity obtained through fMRI.

There are, however, limitations of the study. For one, the sample was very small, and thus it is difficult to generalize the findings. Further, the results showed that it took some time for activities in the brain to decline; there was no clear explanation for this. The question whether endorphins were released during pain modulation or there was a lengthier pain modulation process could not be ascertained limits the findings regarding the precise nature of pain modulation and transmission during placebo use. Despite the limitations, I find the arguments convincing but only in the context of the types and levels of pain stimuli administered, and so far as correlation with fMRI images with pain ratings in a small population is concerned.

There are several other factors which affect pain modulation and pain ratings. Individual pain thresholds, attitudes towards pain and pain relief, participant gender, negative emotions such as fear, and sensitivity to opioids may affect the experience of placebo analgesia as these factors result in different perceptions of pain and variations in modulation. Though these factors have the most significance in studies focusing specifically on placebo efficacy; they can still potentially influence the results of the above study. Nevertheless, the study encourages a more serious look at placebo mechanisms and the ways to hurdle many difficulties involved in its investigation due to the fact that it does not affect the body in the same ways as conventional pain interventions. The study also underscores the human capacity to achieve analgesia even without pharmacologic intervention.

Future research should be directed towards consideration of the other factors that impact the pain processing and modulation as mentioned above. It should also be determined whether findings would significantly change with variations in sample size and sample characteristics. For instance, subsequent studies should increase sample size and incorporate controls for gender. Further, there is a need to resolve the issue of whether individual differences are an innate components of the quality of responses to placebo or whether there are distinct patterns that can be concluded with regards to the many factors involved. This will determine whether findings can ever be generalized in regards to certain populations. Finally, there is a need to find out if placebo can induce pain relief in non-experimentally induced pain such as acute and chronic pain or severe pain associated with illnesses, the aim of which is to establish the limits of its efficacy.

Code: Sample20

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