A German research team has shown that ancient neural pathways in the human brainstem are involved in the 'placebo effect', the well known medical phenomenon that occurs when a patient feels less pain after being given what he or she thinks is a painkiller but is, in fact, a medically inactive substance.

The research results, published in the journal Neuron, provide interesting evidence of how the placebo effect really works and why the expectation that a treatment will reduce pain can actually create that reality.

The placebo effect is thought to be due to a person's belief that a pain-reducing substance has been given to them which will lead to a lessening of pain. How this happens has not been fully explained.

The brain produces substances called endogenous opioids, which play an important role in pain and anxiety relief. These substances have been implicated in the placebo effect. Brain-imaging studies have shown that a feeling of 'placebo analgesia' stimulates the production of endogenous opioids from the regions of the brain that are associated with pain amelioration. The feeling is also associated with a decrease in pain signals.

"It has been hypothesised that placebo analgesia also recruits the opioidergic descending pain control system, which inhibits pain processing in the spinal cord and, therefore, subsequently reduces pain-related responses in the brain, leading to a decreased pain experience," explained leader of the research team Falk Eippert from the University Medical Centre Hamburg-Eppendorf in Germany.

The team used highly sophisticated brain-imaging techniques to examine higher-cortical and lower-brainstem responses in two groups of subjects. One group was given a drug called naloxone which blocks opioid signalling and the other was given a simple saline solution. Both groups were told they had been given pain relievers.

The team found that the drug naloxone reduced the placebo effect as well as placebo-induced decreases in pain-related brain responses. Importantly, they also found that in the placebo group, cortical areas interacted with brainstem structures that are involved in pain control. These interactions were dependent on endogenous opioids and were related to the strength of the experienced placebo effects.

"Taken together, our findings show that opioid signalling in pain-modulating areas and the projections to downstream effectors of the descending pain control system are crucially important for placebo analgesia," said Dr Eippert. "It will be interesting to see whether opioid-dependent activation of the descending pain control system is a common feature of different forms of pain modulation such as hypnosis and attentional distraction, which share some common neuroanatomical features."

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