Back in the early 1600’s, a famous philosopher and mathematician named René Descartes came up with a theory to explain pain.
This theory can be summed up by the painting to the right (created by Descartes himself): a disturbance is passed along a nerve fiber until it reaches the brain. When the brain becomes conscious of the pain signal, it somehow reacts (by moving you away from the fire, for example).
Prior to this, people believed that pain was caused by spiritual or mystical forces. With Descartes new theory, pain finally had a physical explanation.
Innumerable treatments for pain are based on this model of “pain receptors” (nerve endings) detecting damage or degeneration, and sending “pain signals” to the brain. Many people continue to think this way – including a lot of healthcare professionals.
It is thought that pain can simply be “killed” by using medications to numb pain receptors. If pain persists (becoming “chronic”), some sort of degeneration or mechanical problem must exist that continues to aggravate pain receptors, and therefore must be “corrected” through surgery.
How well does this model explain pain?
More importantly, how well do these treatments work?
Medications – a cure all?
Pharmacological treatments (over the counter or prescription drugs) are usually one of the first things used in the fight against pain. But do they even work well?
In many cases, pain medications do work reasonably well for acute pain – the type of pain that typically accompanies some sort of new damage or injury. For example, NSAIDs (Nonsteroidal anti-inflammatory drugs) have been shown to be effective for muscle soreness after exercise 1, injuries (like ankle sprains) 2, and after surgery 3 (such as a knee replacement).
However, not all pain is that simple. For chronic pain, medications (such as NSAIDs, and opioids like morphine) are only slightly effective, with a lot of variation – it works like a charm in some people, and not at all in others. Research studies have shown only “small effect sizes”, averaging about 1 – 2 points of improvement on a 10 point scale. 4, 5 That’s not very impressive!
Of course, it’s been known for a while that pain medications are not magic bullets for pain. That’s why people continue to look for something in the body that’s causing the pain. Perhaps something is permanently damaged, or mechanically out of place?
Using the low back as an example, let’s take a look at the research.
Damage, Degeneration, & Surgery
When people hurt their lower back, they immediately worry that some sort of damage or degeneration has occurred in their spine. Of course, a new injury to the spine will probably cause pain. But when pain persists beyond typical healing times (3-6 months), it’s often blamed on the presence of degenerative changes like bulged (herniated) discs, degenerative disc disease, subluxation, scoliosis, osteoarthritis, pinched nerves, etc., which require surgery to correct.
However, surgery for low back pain has been shown to provide only short-term benefits, that are often no better than intensive rehabilitation, 6 or cognitive-behavior (talk) therapy. 7 For serious conditions that cause disability, surgery is effective for improving physical function 8 – but not necessarily pain. 9 Furthermore, surgery often has the side-effect of causing chronic pain. 10, 11, 12
Obviously, back surgery is extremely complicated due to the complex anatomy of the area, and the fact that things need to be cut in the process. Surgical methods may improve in the future, but it’s certainly no sure-fire solution for chronic pain. But why not? Aren’t these degenerative changes the cause of pain?
Apparently, not so much. Studies using x-rays, CT scans, and MRI’s have consistently shown that the presence of one or more of these ‘problems’ is unrelated to whether or not someone experiences chronic pain. 13, 14, 15, 16 Bulged discs almost always heal (reabsorb) on their own, 17, 18, 19, 20 and even when they don’t, pain still improves! 21
That’s right, you can have a bulged disc or degenerated spine, maybe even impinging on one of your nerves, and still not have pain. Or you could have none of these problems, and still have persistent pain! In fact, people who get MRI’s to investigate their low back pain end up no better than people who don’t. 22 It seems the details of these degenerative problems do not deserve the attention they get.
Then what’s causing the pain?
In September 2012, a study was published in the research journal Arthritis & Rheumatism that looked at the relationship between knee osteoarthritis and pain. 23 The study found people who had a little arthritis and high pain, and people with severe arthritis but low pain. They also tested their pain sensitivity through a number of different techniques.
The results demonstrated that people with high pain / low arthritis had increased pain sensitivity, while those with low pain / high arthritis has decreased pain sensitivity. The researchers concluded that the level of knee pain was due to “central sensitization”, rather than the level of osteoarthritis.
In other words, the level of pain in these people had more to do with changes in their nervous system, not changes in knee structure!
Central sensitization involves the whole nervous system – the nerves in your body, the spinal cord, and especially the brain. We’ll talk about this more in future articles.
Medications and surgery seem to be helpful for pain problems that originate from new injuries, but they are limited in their effectiveness against persistent (“chronic”) pain.
While extreme cases may contribute to some pain problems, degenerative changes might be nothing more than a normal part of aging – and no more painful than the wrinkles on your skin.
It seems that the formula: pain receptors detect damage / degeneration, and send pain signals to the brain – is not quite sufficient to explain pain. This is because damage does not equal pain; not all damage leads to pain, and not all pain is caused by damage. The science of pain is only beginning to make sense. Due to some very exciting scientific progress in such fields as neuroscience and biochemistry, our understanding of pain has increased dramatically over the last few decades.
There are a lot of good reasons why people should learn this new pain science. How pain “works” will be discussed very soon in upcoming articles.
But first, there are a few more myths to bust.
Stay tuned for ‘Outdated Pain Theories, Part II’!
23. Finan PH, Buenaver LF, Bounds SC, Hussain S, Park RJ, Haque UJ, Campbell CM, Haythornthwaite JA, Edwards RR, & Smith MT (2012). Quantitative sensory tests of central sensitization are associated with discordance between pain and radiographic severity in knee osteoarthritis. Arthritis and rheumatism PMID: 22961435