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A swift lesson about PAIN - part three

education nociplastic pain pain Aug 30, 2022
radar screening scanning for threats

The third and final destination in our whistle-stop tour of pain is nociplastic pain, also known as central sensitisation. 

We have covered nociceptive pain – the collection of signals from around the body which might then be determined as painful or not.

We have also explored neuropathic pain - pain from the nerves that are meant to be clear conduits of information.

Nociplastic pain is a slightly more elusive entity, but here goes.


Opening the gates

It has been said that the history of science is science itself. It can be useful to follow the development of knowledge when exploring a subject such as this. Layers build on top of layers.

In the 1960s, two pain researchers, Melzack and Wall proposed a “Gate” theory. It’s a nice model that offers us a view of pain and how it can be increased or suppressed.

We know that sensory signals are gathered around our body, collected in the spinal cord, and passed up to our brains. The pathway is relatively simple, yet we know that pain can depend on context. Someone on a battlefield often experiences less pain than someone dealing with their phobia. Something along the nociceptive pathway from our extremities to our brain can modulate incoming signals, either amplifying or subduing them. Some of this happens in the spinal cord, and this is where Melzack and Wall said there were “gates”.

Obviously, these are not physical gates but are perhaps more like a light switch with a certain amount of stiffness that needs to be overcome to flick from off to on. What Melzack and Wall proposed was that signals from the brain can affect the stiffness of the “gate”, making that switch easier or harder to move.

So should you be on a battlefield and suffer an injury, your brain can send a signal down through your spinal cord that increases the size of any nociceptive signal needed to “open the gate”. This is pain modulation, and we do this all the time. Certain injuries only hurt when we are aware of them and the rest of the time, we subdue them.

Unfortunately, this process can also work in reverse. Signals from the brain can travel down through our spinal cord and leave all our “gates” wide open, or at least make that switch easier to flick. This now means that even the smallest signal from the periphery gets through when perhaps it wouldn’t under normal circumstances.

Patients start to feel an obvious exaggeration of their pain, or in some cases even experience the lightest touch as pain. This can be temporary, or even permanent.


Who left the door open?

Remember the three nerves we talked about? The first nerve from our periphery passes signals to our spinal cord almost continuously. We now know that there should be a selective process of sorts so that only signals above a given threshold pass to the second nerve and onwards to our brain. But if the “gate” is left wide open, that second nerve is bombarded with information, relentlessly. The threshold has been lowered, and everything is now getting through.

This model of pain was called central sensitisation, as the central structures of our pain network, the spinal cord up to the brain, are now overly sensitive to inputs. It’s not a great position to be in, as innocuous signals can now enter our nervous systems and deliver more of a kick than was really intended.

The obvious question at this point is whether there are people with easily opened gates, who are very sensitive to pain. In contrast, are there people with “stiff” gates, who therefore have a higher pain threshold? We all know some examples of people at either end of the spectrum, don’t we?

We can also now comprehend how our own pain experiences might vary. It’s good to stay busy if you’re in pain, and that’s because focusing attention on tasks seems to close our gates. In contrast, when people talk about a pain you have, the discussion can seem to make your pain worse. Your gates get opened thanks to your attention being directed towards the injury.

Now we have a theory that explains modulation of pain, we need to think about what might trigger these modulations.


Onwards and upwards

The more recent history of pain research has been focused on the role of the brain. Our understanding of pain through time seems to have followed the course of our nervous system from out to in, and we are now learning more about the central processing of what we feel.

To skip a few decades of research, let’s jump to the understanding that there are very few parts of our brain that aren’t involved in our appreciation of what is around us, and therefore have something to contribute to our experience of pain or the lack of it.

Pain, in its essence, is a protective system. It exists to prevent us from causing further damage. Our nervous system senses the world around us, thinks about what is going on, and helps us decide what to do.

If we use the analogy of a burglar alarm, we rely on sensors to detect what is happening, and on computing to tell us where it is and what it might be. Sometimes, the errors in our pain system are akin to a movement sensor that has lost its calibration. A burglar alarm should be triggered by a human figure moving past it, but not by a fly buzzing around the room.

Similar to this, our nervous systems can overreact to relatively innocuous signals. In certain conditions, we can set alarms off in adjacent rooms (referred pain) if we are sensitised enough. Furthermore, once an alarm has been set off, our nervous systems can sometimes get stuck in that state, something like a short circuit.


What causes the fault?

If you put someone in a brain scanner and then do something painful to them, you will see most of their brain light up. Not just the part of the brain that we know is related to sensation. It's too crude to say that one particular fault can cause pain to be amplified or prolonged, but rather, we must appreciate that many factors can contribute. Some examples include:

  • Our past experiences of pain – our memory. We might be expecting a repeat of a previous pain experience, and “fast forward” to what that felt like, even though the repeat injury is nothing like as bad.
  • What people tell us can also have an impact. If friends or family tell you their tales of woe, it can lead to a greater sense of threat. We empathise with them and start to imagine what they must have felt.
  • A similar nocebic process (the opposite of placebo) can be initiated by therapists who inadvertently make patients feel worse by explaining what is going on and what might happen next. They might be trying to protect their patients, but sometimes an over-enthusiastic sharing of knowledge can paint a negative picture.
  • People sometimes have their own negative opinions of what might be around the corner. Perhaps these people are pessimists in general but this can lead to them suffering from increased and prolonged pain. Their brains are halfway there already.
  • There are also some very important social determinants of health. Social background, levels of education, wealth and access to resources all have an impact on how people experience pain.
  • Last, an interesting group are those who sleep badly. Bad sleepers are more likely to experience pain in excess of what it perhaps should be. People with pain also tend to sleep badly, so there is a vicious circle there.

It's fair to say that there are many ways in which pain experiences can vary and be altered not just through our "gates", but also within our individual environments and last, due to the fact that we are all wired differently.

This is a good point to consider that the word "plastic" means something which is shaped or moulded. What we are seeing through this blog is how nociceptive signals cause changes to brain structure and function. They induce a form of plasticity - creating changes. We should also remember that neuropathic pain can also cause plasticity in our brains, leading to prolonged and exaggerated "states of pain". If anything, neuropathic conditions are a more powerful contributor than nociceptive signals when considering nociplastic pain, but let's leave that there for now.

Last, let's look at how our body fluctuates from rest to alarm and the relationship with pain.


A permanent adrenaline rush

The common result of a fixed state of pain is a constant state of alarm.

You know what an adrenaline rush feels like and what it can do to you. Just about every part of your body adjusts its function, either increasing or decreasing what it does as we respond to our surroundings.

On a normal, pain-free day, we typically fluctuate gently between a sense of safety and relaxation and a state of mild alarm and occasional fear. When we have pain, however, we get pushed in one direction closer to a constant state of alarm as we try to protect ourselves from danger.

That danger might be smaller than we think, or even a memory, but the state of fear in our brain can help open the “gates” in our spinal cord allowing signals to pass through more easily. The incoming signals that then get through will further influence the activity of our brain, raising our perception of threat.

The vicious circle is complete.


Can we break the cycle?

For nociceptive pain, we have medications that reduce inflammation or “numb” our brain into ignoring the signals temporarily.

With neuropathic pain, certain drugs help the nerve tissue function better.

When we are dealing with nociplastic pain, we want to break the cycle that has formed within various centres of our brains.

Something is a threat so we should increase our sensitivity to incoming signals. Oh wow – those signals are strong – the threat is real so we should increase our sensitivity to incoming signals…

And so, we have various classes of medication that act to suppress brain activity. That sounds scary, but used properly, and under expert guidance, these medications can help patients get away from their constant state of pain and alarm. Their success is, however, a bit of a mixed bag and there is commonly a process of trying different combinations and doses of medications. Not the exact science we’d all like it to be.

The non-pharmacological routes to helping such conditions are based on tactics that calm our brains. Mindfulness is a powerful way of regaining control of a brain that is constantly seeking fear and producing a sense of panic. Breathing techniques are also a great way of slowing our systems down and breaking the vicious circle. These methods help us return to a calm state, not the fear and flight that helps amplify our threat perception. Our alarm sensors can now recalibrate and should not get set off by that pesky fly anymore. At least, that's the theory.


Done? Not done…

This is the end of a whistlestop tour of pain, looking at three main areas.

Three blogs have probably been enough for most people, but each sentence in them is the life’s research of someone in the field of pain science. It’s a fascinating area, not common knowledge, but we are hopefully entering a world where better-informed practitioners can help those in pain with a more subtle set of tools, not just a massage and a machine that goes “bing”. Or at least, let’s hope so.

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