My gaze swung between the man on the exam table and the radiograph displayed on the lightbox. He must have sensed a problem.
“What?” he asked.
What indeed. The film basically showed his shoulder blade broken in two.
“When did this happen?” I inquired. He had already told me once; I just needed to be sure that I’d heard it correctly.
“Yesterday afternoon,” he said, ” right after lunch.”
“And why did you wait until this afternoon to come in?’
“Well, I’m here mostly to get my wife off my back. If it was up to me, I wouldn’t have come in, but she thought it might be serious or something, because I tossed and turned last night.”
“Well,” I told him, “It is not a surgical problem, but it is a bad injury. You got lucky.”
After a moment’s reflection I added, “Didn’t that hurt?”
“Kind of,” he laughed, “But it eased up pretty quick.”
“Do you need any pain medication?” I asked.
“Oh, no,” he demurred, “Tylenol is doing fine for it.”
After a few more pleasantries, the man got up, walked out of my office, got in his car and drove back to work. Watching him wince slightly as he turned out of the parking lot, I couldn’t help but think of the patient before him – a fellow with no history of serious injury, a normal MRI of the lumbar spine, and disabling back pain.
The man with the back pain had wanted pain medication. I’d had to talk him out of it, which was a difficult task in that era. Because it was the era before the opioid crisis, when we were in the midst of a pain crisis, according to the medical authorities. Clinicians were directed to take everyone’s pain level the same way that we took their temperature, and to treat the abnormalities discovered by our measurements.
For those with eyes to see, the notion behind pathologizing pain was misguided, at least. The whole scheme rested on the idea that pain was simply activity in the neuronal substrate. Change the activity pattern, by activating opiate receptors, for example, and you get rid of the pain.
I am not being very charitable in my description, but I am being as charitable as I need to be. There are more nuanced depictions, which leaven the mix with talk of psychological context and so on, but the same suppressed premise lurks beneath them all. It is this: a chain of causal events ‘add up’ to pain, and that is just what pain is. X+Y+Z = Pain. But the necessity of such arithmetic has been in doubt even before Hume laid its troubles out so nicely for us Westerners.
Breaking down a phenomenon gives you its pieces, but does not grant commutativity. Activating opiate receptors does not reshape their owner’s pain experience according to a fixed script. Receptor activity is part of the description of a painful experience, along with psychological context, and personal history. Yet there is no prior necessity – necessity by law, rather than necessity in fact. We did not make the distinction.
Secure in our estimation of the relationship between the neuronal substrate and the pain experience, we went after opiate receptors like we go after splinters. Our efforts did not force anyone’s pain experience into a box, but we gave everyone who we treated a new pain experience. Sometimes it suited them better; sometimes it suited them worse. Many, many times it settled in the center of their psyches and they fell into orbit around it.
Our engagement with the epidemic of untreated pain predictably ended in chaos. Now we need to extricate ourselves, and what do we turn to but the tool already in hand.
Instead of the reduction to type, we have rebuilt our story of pain, revising our reduction on the basis of the same mistake. Receptors pertain to behaviors – in the neuronal substrate, and so in the psychology, and so in the organism – but pain is a byproduct of the behavioral mechanism. It is an epiphenomenon. Chronic experiencers need counselling, to convince them that the pain is ineffectual, and therefore not real, at least not in any serious way.
Unfortunately, I get to participate in this second shot at commutative reduction, too. It will go just as well as the first.