We always bump into this. There we stand, trying to figure out what is causing the patient’s pain, and the patient says “So – what is causing my problem?”. And we suddenly realise that what we want to say (for example, the way we might explain the problem to a fellow practitioner) is entirely at odds with the way that the patient can understand it. Of course, experienced practitioners know that the simplest thing to do is to answer in ways that the patient can ‘see’ (or hear, or even feel – whatever their modality of thinking).
But we also need to structure our own thoughts about what seems to be happening, and why. For this, we need to bear two concepts in mind. First, what appears to be the sequence of cause and effect? This linear way of thinking about spinal function and dysfunction has merit, but may also be sneakily deceptive. Second, thinking about the problem as a system – where multiple interacting factors generate spinal dysfunction as a failure of adaptation – and where we are more interested in the integrity of coping mechanisms.
So the following is a few ideas about all this.
Looking at it from the patient’s point of view, the vast majority just seem to want to know what is actually hurting – not even what is causing the hurt. So if they have the dull ache of fatiguing, tired erector spinae, they want to hear that their muscles are aching (lumbago is an excellent word for this). If one tells them that their muscles are damaged and sore, then even better – because they can make a connection between damage and pain. But they do seem to be far less interested in the ultimate causes of their discomfort.
There are many reasons for this, of course, including;
- their fears and apprehensions
- whether the patient is active or passive about the health and functioning of their body
- whether the patient sees their body as an ‘it’ or as part of their own responsibility
- and so on
When it comes to communicating the nature of the problem to the patient, it is useful to have formed a quick assessment of where they are coming from. Irrespective of your diagnostic or technical expertise, a patient’s impression of how good you are seems to depend heavily on whether you ‘made sense’ or not!
Having said all this, what then matters to us is making some decisions. To start with, we could use the following approach. Decide whether;
- damaged tissues are generating pain through inflammatory mechanisms or
- non-damaged tissues are causing pain through non-inflammatory mechanisms (muscle fatigue, even some types of ligamentous nociceptors)
In the first case, we need to decide if the structure was damaged by an extrinsic injury. E.g. “I was kicked in the back playing soccer”. Or, by an intrinsic fault of spinal functioning. E.g. a sitting patient suddenly looks to the right, and because of excessive muscle tension below the cervical area, abnormally rotates and tears some of the capsular fibres of a facet joint in their neck.
But in both cases of damaged tissues, we are primarily interested in the healing rate of the patient, and how we can – either through treating or advising the patient – speed up this healing rate.
In the second case of non damaged tissues causing pain, we are not so much interested in tissue healing rates, but rather in how we can alter spinal functioning in such a way that the abnormal excessive load on the structures generating the pain is reduced enough to ‘give them a break’.
If we do this accurately, some patients can respond immediately with a sense of ease and symptom reduction, whereas for others it can take a while for the spinal system to re-adapt. Age, length of time with the problem, general health and vitality and the presence of pre-existing patterns all play a part in this re-adaptation rate.
Then we can consider the multi-factorial nature of most problems. For example, take a migraine pattern where some factors (e.g. spinal posture, foods, alcohol, psychological stress) all combine as a pattern generator for a migraine. Very probably, there is a trigger ‘threshold’ which, if reached by the addition of these factors, will spill over into an episode. Imagine in a patient that the sum of the combining factors is just below the symptom trigger threshold, but then an increase in the intensity of one of these factors, or even the addition of a smallish new one, trips the pattern into symptom mode.
In this example, what is the problem? The pre-existing factors, or the new one? Clearly, this is a ‘straw and camel’s back’ type of question. But any proper answer to the question is more than just semantics or of difficulty in communicating these concepts to a puzzled patient. Why? Because thinking about these things allows us to decide where we can help, and where we can assist the most.
So when a patient asks us “so, what’s my problem?” – is it any wonder we – most of the time – have to simplify?