A pathway to control pain

Studies have previously shown that the injection of lidocaine into the rostral ventro-medial medulla (RVM) in the brainstem decreases neuropathic pain. This was attributed to lidocaine selectively blocking a descending pain-facilitatory system.

However, a group of researchers from Lebanon challenged the facilitatory concept in a research paper that looked at the effect of injecting different concentrations of lidocaine. A high concentration led to a decreased sensitivity to pain, whereas a low concentration had the opposite effect. The researchers then coupled the lidocaine injections with those of gamma-aminobutyric acid (GABA) and glycine agonists and antagonists in groups of rats. Injecting an agonist was found to decrease the effect observed when lidocaine was injected alone. Injecting lidocaine after an antagonist showed no further change in the pain response.

The paper explains that the agonists counter the inhibitory effect of lidocaine on neuropathic manifestations, whereas an injection of lidocaine with an antagonist showed no change because they were competing for the same target.

This suggests that, rather than affecting a facilitatory system, the injection of lidocaine shuts down the GABAergic and glycinergic inhibitory neurons in the brain, which in turn releases a pain-inhibitory system. This also explains why the effect of lidocaine is dose-dependent.

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