There we are, trying to figure out what’s causing the patient’s pain, and they suddenly ask, “So what is my problem?”
With a start, we realise that what we want to say is entirely at odds with the way that the patient can understand it.
Of course, experienced practitioners know that the best thing to do is to answer in a way that the patient can see, hear or even feel. Whatever best suits their modality of thinking.
It’s not easy switching from evaluation mode to seeing things from a patient’s point of view, having a chat with them, making sure they are happy, then switching back again. The more anxious the patient, the harder this is.
How do patients see things?
If they have the dull ache of tired erector spinae, they want to hear that their muscles are aching and that the ache does not have a sinister cause. Lumbago is a useful term for this.
If one tells them that their muscles are damaged and sore then even better. Why? Because they can then make a connection between damage and pain.
Generally, they are less interested – at that moment in time – in the ultimate causes of their discomfort. Trying too hard to make them see things from our point of view is often counter-productive.
There are many reasons for this, including lack of time, fears and apprehensions, whether the patient is passive about their health, whether the patient talks about their body as an it, and so on.
That’s why, when discussing the nature of the problem with the patient, it’s sensible to understand how they see things, and how they can see things.
Irrespective of your diagnostic or technical expertise, a patient’s impression of how good you are seems to depend heavily on whether you make sense to them – or not.
After all this, I try to choose between two different ways of thinking about the patient’s problem.
Cause and effect versus systems theory
First, what appears to be the sequence of cause and effect? This linear way of thinking about spinal dysfunction has merit, in that it allows us to recall and structure our knowledge, but it can also be quite deceptive.
Second, should we view the problem as a systems problem? Here, many interacting factors generate spinal dysfunction as a failure of adaptation. Rather than focusing on causes, we become more interested in the capacity of coping mechanisms.
Ultimately, the spine is itself a coping mechanism. It manages the forces of gravity, of linear and angular momentum/acceleration, and the effects of the passage of time.
Having said all this, what matters is making broadly correct decisions.
To start with, we could use the following approach. Decide whether;
Non-damaged tissues are causing pain through non-inflammatory mechanisms (e.g. muscle fatigue, ligamentous nociceptors).
Or damaged tissues are generating pain through inflammatory mechanisms.
In the case of damaged tissues, decide if they were damaged externally or internally. For example, a kick in the back while playing soccer is an externally generated injury. A laptop warrior who strains a facet joint when he rotates his neck has an internally generated injury.
Although it’s usually evident from the case history, it’s good to be clear about the difference, because the possibility of significant harm is so much more in the former.
For both these causes of damaged tissues, we are primarily interested in the healing rate of the patient, and whether we can speed this up, either through treating or advising the patient.
For painful but otherwise intact tissues, once we are sure there is no systemic inflammation complicating matters, we need to alter spinal functioning in a way that reduces abnormal loading.
If we do this well, patients respond with a sense of ease and symptom reduction, though for some it can take a while for the spinal system to re-adapt.
Age, length of time with the problem, general health, vitality and fitness, and the presence of pre-existing patterns, all play a part in this re-adaptation rate.
Most problems have a multi-factorial nature. Consider a migraine pattern.
Factors such as posture, foods, alcohol and psychological stress all combine as a pattern generator for a migraine.
There likely is a trigger threshold which, if reached by the interaction of these factors, spills over into an episode.
An asymptomatic patient hovering just below the symptom threshold who has an increase in the intensity of one of these factors, or the addition of a new one, will trip into symptom mode.
In this example, what is the problem?
The pre-existing factors, or the new one?
This is a straw and camel’s back type of question which neatly illustrates why linear cause-and- effect thinking has limitations.
Patients, not unreasonably, focus on the catalyst. For example, strawberries. But that’s quite a limited way of understanding, and certainly of managing, the condition.
Any proper answer to all this is more than semantics or about the challenge of explaining concepts to a puzzled patient.
Why? Because thinking as clearly as possible about these things allows us to decide where we can help the most.
And when a patient asks us what the problem is, is it any wonder that – most of the time – we need to simplify?