Medical experts love getting together and negotiating consensus positions for diagnostic and treatment guidelines and definitions. For example you are considered to have persistent (previously known as chronic) pain when you pass the three month mark from the onset by the official consensus-reached-by-many-experts conclusion. Furthermore you are entitled to ‘normal’ pain due to proportionate nociceptive (electrical signalling) stimulus in the early injury phase always, and there is no reason to have any concern unless that pain persists.
ie- like this lovely commonly used graph picture:
(It is easier to see the details if you click on it)
I suppose this makes practical sense, for example so that epidemiologists (researchers in health statistics) can analyse things.
The actual guidelines are more intricate if you read them carefully ie via: http://www.apsoc.org.au/PDF/Position_Paper/apa_position_statement.pdf but I can tell you from multiple conversations with a biomedical model obsessed therapeutic community that there is a problem. What is actually practically remembered by most is that somehow maladaptive pain is only really a consideration after 3 months and even after that the scan changes seem to dominate anyway until everyone gives up on ‘fixing’ things a long way down the track.
What inevitably happens is that people then think the consensus derived definition is sacrosanct and direct more energy into defending the definition and pigeon-holing people into it than managing the actual highly complex situation in front of them.
Now let me show you how easily this approach comes unstuck.
Let’s keep on track and consider that lovely graph above. (Again, it is easier to see the details if you click on it)
Keep the thought of those red and yellow lines running perfectly together in the early phase following “the moment of injury” and now have a look at what I call – “A tale of two nails”.
A tale of two nails – ‘Perception is everything’
Reference: A Biological Substrate for Somatoform Disorders: Importance of Pathophysiology. Joel E. Dimsdale, MD and Robert Dantzer, DVM, PHD. Psychosom Med. 2007 December; 69(9): 850–854:“Two brief case reports involving construction injuries with nails demonstrate the phenomenon beautifully. In one report (6), Fisher et al. described the case of a builder who jumped down onto a 7-inch nail, which pierced his boot at the toe level (Figure 1, left panel). The man was in pain and required intravenous sedation in the emergency room. However, when the boot was cut away, it turned out that the nail had fortunately passed between his toes as opposed to its apparent impaling of the foot. The man’s agonizing pain was elicited solely by his misperception—a case of somatic amplification. On the other hand, a report in USA Today described a construction worker who had unknowingly shot himself in the head with a nail gun (Figure 1, right panel) and who was unaware of the injury. He perceived a toothache and went to a dentist 6 days later, wherein the cause of the rogue toothache was discovered. In this case, one would conclude that somatic deamplification was at work. The patient was unaware of the injury and attributed the sensation to more familiar sources.”
In plain speak all this translates to the first dude thinking he was injured and having severe pain until he realised he wasn’t actually injured and the second dude being injured but because he wasn’t aware that anything happened, he generated no acute pain response.
This makes a bit of a mess of the lovely early bit of the graph, doesn’t it?
Another lovely example of this is Lorimer Moseley’s ‘snake bite’ story (check out the you tube video directly or via the ‘For Patients’ page on my website if you haven’t been to one of his lectures yet).
So, you may be saying – Why is this important? Why can’t I have my lovely little graph and definitions? Why are you making my professional life so difficult? Please go away and leave me alone!
The problem is this – firm adherence to linear definitions in what we know is the extraordinarily complex and multi-factorial construct of PAIN is in itself a contradiction in terms. The biomedical model view is based on a fundamental flaw which is the absence of a linear relationship between structural changes and pain. I urge the pain fraternity not to inadvertently make the same fundamental error. NB: People rarely read the fine print, so the message has to be very clear. The pain is either positively adaptive or negatively maladaptive and the earlier that is considered perhaps the better, albeit being cautious not to miss any ‘red flags’.
A practical example of this problem is a conversation had recently with an eminent spinal surgeon who advocated earlier surgical intervention for back pain on the basis that he was trying to avoid the persistent pain ‘phase’ after 3 months!!
Practically this problem is also manifest so very commonly by cases that I am involved with in compensation reviews where the ‘punishment just doesn’t fit the crime’.
These cases regularly involve minor mechanisms of injury with extraordinary long term and tragic pain outcomes. These problems are even potentially cross generational and the flow on effects in terms of social breakdowns, costs to the health system etc, etc, etc are well known.
In fact, it is my regular observation that, paradoxically, those with more severe traumatic injuries seem to recover better (in the absence of an acquired brain injury component) than those with minor ‘eg: I tweaked my back’ type injuries. There is that contextual and motivational influence again …
In an alarmingly large number of cases the original mechanism of injury leading to persistent pain in a ‘someone to blame’ context is almost the equivalent pathophysiological trauma of being blown over by a feather. There is a stark contrast to similar and very much more severe trauma occurring in a sporting environment.
Now that is not to say that there is no electrical signalling input to a protective pain response at all, ever. That is not what I mean at all. I am sure that even in the first nail case above, the electrical signalling from the nail passing frighteningly close to the tissues was appropriate to create that protective response saying ”help!!’ It is just that it proved to be a maladaptive response right at the very start of the problem and luckily it could be proven objectively once the shoe was removed.
To conclude, please consider an analogy with the first nail case. Imagine the shoe to be the external body covering of the spine. Then imagine the nail to be the ‘tweak’ of sudden pain lifting, bending or similar in the back, stretching briefly those poor little previously well adapted nerve roots or similar. Imagine the same early protective pain response. Imagine further that instead of being able to take the shoe off and prove that there was no reason for alarm and further protective pain, someone told you that the nail was stuck in your foot, or in spinal terms, you have got a disc ‘bulge’ / ‘pars defects’ or ‘fractures’ / ‘spondylolisthesis’ / ‘instability’ (isn’t that a common one these days?) etc, etc, etc ………….
Actually, you don’t have to imagine this at all; it can be seen so very often.