https://www.ncbi.nlm.nih.gov/pubmed/301658
Relief of intractable pain was produced in six human patients by stimulation of electrodes permanently implanted in the periventricular and periaqueductal gray matter. The level of stimulation sufficient to induce pain relief seems not to alter the acute pain threshold. Indiscriminate repetitive stimulation produced tolerance to both stimulation-produced pain relief and the analgesic action of narcotic medication; this process could be reversed by abstinence from stimulation. Stimulation-produced relief of pain was reversed by naloxone in five out of six patients. These results suggest that satisfactory alleviation of persistent pain in humans may be obtained by electronic stimulation.
The crux of the question is asking, if the patient feels decreased pain (which is driven by opioid molecules; that's why opioids are administered as painkillers), then how do you stop the inhibition? An opioid antagonist (naloxone is the only one that is an antagonist)
submitted by โwaterloo(126)
if you look at the answer choices, they are all pain suppressors except for naloxone.
Naloxone is an opoid antagonist so blocking mu receptors would lead to increase in mediators that induce pain.
I don't think you need to know any experimental data, or really anything before the last two sentences. He is given something that reduces pain (opioid agonist), and if you give him naloxone you would be reducing the effect of his opoid agonist.