A recent study looked into the neural functions affected by ibuprofen and found some connections that may soon lead to a much greater understanding of the greatest pain mitigator of them all: the brain.
You don’t have to be a pain management specialist to know that ibuprofen treats many kinds of pain effectively. But…how does ibuprofen mitigate pain? For that matter, how do any opioids or nonopioids mitigate pain?
Aside from some basic understanding that the analgesic effects of most nonsteroidal anti-inflammatory drugs (NSAIDs) are explained, in part, by the pharmacological property of inhibiting prostaglandin biosynthesis, surprisingly little is currently known about the effect of pharmacotherapy and other treatment strategies on the central mechanisms of pain and inflammation in humans.
An interesting study in Pain looked into the neural functions affected by ibuprofen and found some connections that may soon lead to a much greater understanding of the greatest pain mitigator of them all: the brain. In short, the study looked at the therapeutic outcomes of ibuprofen treatment in the context of endogenous pain modulary systems that emanate from the spinal cord and the brain.
To evaluate the subjective experience of pain and examine the analgesic interaction between surgical state and treatment, the researchers used an established clinical pain model involving third molar extraction (TME), and quantitative arterial spin labelling (ASL) imaging to measure changes in tonic/ongoing neural activity.ASL is an MRI technique that measures regional cerebral blood flow (rCBF).
TME patients are ideal for this kind of research because the subjects are of relatively normal health and are not typically being treated for pain, the surgical procedures involved are standardized, and there are large number of patients from which to choose. This novel methodology was incorporated into a randomized double-blind placebo-controlled design, with an open method of drug administration.
According to the study authors, “We found that independent of its antinociceptive action, ibuprofen has no effect on regional cerebral blood flow under pain-free conditions (presurgery). However, in the postsurgical state, we observed increased activation of top—down modulatory circuits, which was accompanied by decreases in the areas engaged because of ongoing pain. Our findings demonstrate that ibuprofen has a measurable analgesic response in the human brain, with the subjective effects of pain relief reflected in two distinct brain networks.”
What’s new and important here is the identification of a specific network of brain regions that is activated in response to ibuprofen-induced analgesia. “Our finding of an effect of ibuprofen in the presence of postsurgical pain and inflammation suggests that there may indeed be a central component to ibuprofen’s action that is most effective in modulating nociceptive transmission when central sensitization is present,” the authors noted.
The researchers hope that the study sparks a renewed interest in studying the inhibitory mechanisms of analgesia that can be exploited to improve pain treatment. “Our findings demonstrate that ibuprofen has a measurable analgesic response in the human brain, with the subjective effects of pain relief reflected in two distinct brain networks. The observed activation of regions involved in descending modulatory control is a unique finding that warrants further investigation because this may provide new insights into the inhibitory mechanisms of analgesia.”