Types of pain – Clinical application

(Below is the trascript of the video above)

Knowing what type or types of pain someone has is not much use if you don't know how to use the knowledge and clinically reason your way to an effective management. In today's video I'll attempt to briefly explain what it all means.

It's necessary to know the types (or more accurately "mechanism") of pain, simply because each type of pain has different physiology that is driving the pain, and thus requires different interventions or INTENTION behind interventions. But first, we need to recognise different mechanisms of pain when we see one.

For example:

- a 1-day-old ankle sprain is probably full of inflammation, whereas pain four months after a sprain is more likely to be dysfunctional.

- a chronic neck pain may be to do with central sensitisation which is dysfunctional, or muscle insufficiency which may be more nociceptive.

- a carpal tunnel syndrome may be quite neuropathic and inflammatory, or it may be more dysfunctional.

- a back pain could be nociceptive due to the pain straight from a disc that's been stressed beyond its adaptive capabilities , it may have a neuropathic component if it has an acute nerve root compression, and if chronic it may be dysfunctional due to central sensitisation. There may even be some inflammation around the area as well.

And of course, in most cases it's a mixture of the these four mechanisms of pain. It's simply a matter of recognition and prioritising.

Then how do we recognise the different mechanisms of pain of a given person? That is a pretty big question, and while there are some typical presentations or patterns for each mechanism of pain I just can't go into it in this video.

Same with proposed interventions for pain. It's a big topic with complex and conflicting evidence. We must also acknowledge that perspectives, working paradigms and biases vary greatly across health disciplines AND within each discipline as well, so a same patient can receive quite different treatments from different clinicians and it's very difficult to say who is right and wrong.

However what I can say is that it would be wrong NOT to consider these four mechanisms when caring for patients with pain. At least an attempt at differentiating them will give us much clearer picture of management pathway.

And then we must decide whether the particular mechanism or mechanisms of pain actually needs active management (since most pain self-resolves), and if it does need management how we, the clinicians can positively influence it, with firm consideration of multidimensional nature of pain (1,2).

References

1. Melzack R, Katz J. Pain. Wiley Interdiscip Rev Cogn Sci. 2013;4(1):1-15.

2. Borrell-Carrio F, Suchman AL, Epstein RM. The biopsychosocial model 25 years later: principles, practice, and scientific inquiry. Ann Fam Med. 2004;2(6):576-82.

Types of pain – Dysfunctional pain

(The following is the transcription of the video above)

It is generally accepted in the branch of pain medicine that there are four types of pain: nociceptive, inflammatory, neuropathic and dysfunctional (1-3). The first three have been discussed in previous videos and in this video we'll discuss about dysfunctional.

Dysfunctional pain is tricky to define AND to understand, some will even say that it does not exist. Regardless, let's start with the definition of dysfunctional pain: dysfunctional pain is pain experienced when there is an error in pain processing ability of the body.

This means that there's likely to be NOTHING that's structurally wrong with the patient; X-ray will be normal, MRI will be normal, blood test will be normal, and your muscles and joints and fine. And you might be thinking “hang on a sec, how can you have pain without something wrong with me?"

Well I'm not saying that there is NOTHING wrong with you; it's just that where it's gone wrong is not something that can be SEEN. And THAT is the pain processing centres of the body.

I'll give you an example. Let's say that you've just cut yourself on your finger, it hurts right? I'm sure you can remember that searing pain that is when you've just cut yourself. And that's perfectly normal to feel pain. Now, how long does it take for that initial pain to settle? Maybe ten minutes? Thirty if it's particularly bad.

So when the pain has settled after ten minutes or so, does that mean that your cut has been healed? Not at all, it might take at least a day to really heal up.

So, why does your pain reduce so significantly so quickly, unrelated to actual healing? There are a number of reasons for this but one of the major ones is our pain processing centres. They go - "oh look, a cut on my finger. It's just a cut. I'm sure it'll be fine". Then turn down the initial spike of pain pretty quickly. And this all happens without you being quite aware.

But what if that "turning down the pain" by the pain processing centres does NOT occur? The pain will persist, quite unreasonably, even well after the cut is healed. That's dysfunctional pain. Pain that persists because of errors in our pain processing ability.

Sometimes this occurs even without a particular injury per se. In fact it's most common that this unreasonable persistence of pain occurs from gradual build up rather than one-off trauma. Think chronic back and neck pain, shoulder pain, tennis elbow, most overuse injuries, headaches, irritable bowel syndrome, fibromyalgia, the tension that you feel when you're anxious or stressed, the list goes on.

For now, the most crucial thing for you to understand is the very existence of dysfunctional pain, how it can manifest without any visible structural abnormalities, and how common it actually is.

In summary, there are four types of pain: nociceptive, inflammatory, neuropathic and dysfunctional. What does that mean in real life and how do we apply this concept? That is a pretty big question, and I'll try to explain it some degree in the next video.

References

1. Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci. 2009;32:1-32.

2. Vardeh D, Mannion RJ, Woolf CJ. Toward a Mechanism-Based Approach to Pain Diagnosis. J Pain. 2016;17(9 Suppl):T50-69.

3. Woolf CJ. Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management. Annals of Internal Medicine. 2004;140:441-51.

Types of pain – Neuropathic pain

(The following is the transcript for the video above)

The third type of pain that I want to talk about is Neuropathic pain.

Neuropathic pain occurs when you have pain because there is some sort of a damage or stress to our nerves (1). Now this can sound awfully like nociceptive pain that we discussed two videos earlier, where certain nerves called nociceptors get simulated and send signals to our brain that can be interpreted as pain.

The difference is, in nociceptive pain, the nociceptors are responding to stresses to SURROUNDING structures, like ligaments, muscles, or bones. Neuropathic pain occurs when the nerves THEMSELVES are compromised, and begin to behave rather irritably.

For example, in shingles, a virus attacks the nerves in our spinal cord, and consequently you'll have pain, and even blisters, wherever that nerve goes. Some with diabetes develop peripheral neuropathy where the nerves in the hands and feet become compromised.

And one of the most common neuropathic condition is "sciatica" where the nerves that come out of the spine to supply one of the legs become compressed by something - usually a bulging disc.

It is also probably worthwhile to mention that when this does happen there are effectively TWO conditions that we're dealing with - a bulging, unstable disc, AND an angry, irritated nerve.

That means even if you have a surgery to slice off the part of the disc that's pushing on the nerve, the irritated nerve does not always resolve automatically and THAT may require some separate attention. Something like carpal tunnel syndrome is similar in that regard.

So these are the most critical aspect of neuropathic pain:

1) neuropathic pain is a separate entity to the condition itself. The condition, like shingles, may have passed, but the pain might remain. It's not like where you break a bone and the bone's fixed and you'll be ok. The PAIN needs to be looked at separately (2).

2) the behaviour of neuropathic pain is not as predictable as the previous two types of pain. In nociceptive and inflammatory pain, the resolution of the pain is pretty consistent with a number of factors. Neuropathic pain, often is not so.

3) and lastly, and this is more for the health professionals, neuropathic pain needs to be intervened quickly.

So if you see someone with a suspected bulging disc and raging sciatic pain, don't just settle for finding a solution only for the disc, you must treat the neuropathic pain separately, and AS EARLY AS POSSIBLY, before alterations in neuroplasticity and in gene expressions occur both of which will prolong the pain very much unnecessarily (3). And this multimodal and mechanism-specific approach applies to most neuropathic pain conditions.

References

1. Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci. 2009;32:1-32.

2. Woolf CJ. Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management. Annals of Internal Medicine. 2004;140:441-51.

3. Jensen TS, Finnerup NB. Allodynia and hyperalgesia in neuropathic pain: clinical manifestations and mechanisms. The Lancet Neurology. 2014;13(9):924-35.

Types of pain – Inflammatory pain

(The following is the transcript for the video above)

The second type of pain that I would like to talk about is, pain due to inflammation.

Inflammation is a chemical reaction, that usually occurs when there is a damage in our body. Let's say, an ankle sprain. Initially you'll feel the nociceptive pain of mechanical origin, of the ankle being twisted or ligaments being torn.

Then, if the injury is great enough, inflammation will occur. It's a chemical reaction where certain cells in our body release what we call inflammatory mediators.
And these mediators cause two major consequences:

First, it causes the blood vessels to increase in size, and the plasma in the blood goes out of the blood vessels and into the tissue space, which is essentially space between our tissue cells like muscles and fat. The result is swelling.

Secondly, the inflammatory mediators stimulate the nociceptors around the injury site. So you'll end up with that constant, throbbing, achy pain that accompanies most moderate to high level sprains or injuries.

However, this sort of inflammation does not last long. Maybe three to four days in most musculoskeletal injuries. It literally sorts itself out. Right amount of inflammation is helpful to healing as well.

But sometimes, things can go south. I'm not sure if you can have too little an inflammation, but you can definitely have too much. Also, you may have unnecessarily excessive response from your nociceptors resulting in unreasonable amount of pain.
You could also have chronic inflammation, which is quite different again.

The take home message is, acute inflammation in the realms of musculoskeletal pain (so, not like appendicities), usually follows a decent trauma and is self-limiting.
This means that a lot of chronic pain, like fibromyalgia or chronic back or neck pain, has not much to do with acute inflammation and will not respond well to anti-inflammatory drugs.

Of course there are so much more to this, like systemic inflammation, chronic inflammation, and visceral inflammation and they are all quite different. It is really upto the critical eyes of a competent health provider of your choice who can say how much portion of your pain is due to inflammation, and what can be done about it.

Types of pain – Nociceptive pain

(The following is the transcript for the video above)

In the introduction video I mentioned that pain that you're experiencing does NOT have to equate to physical injuries or deformities. But often it DOES as well. The thing is, that there are different TYPES of pain and identifying which one or ones you're most likely to be experiencing, is absolutely crucial to the management of your pain.

According to Prof Clifford Woolf of Harvard Medical School, there are four types of pain (1,2): Nociceptive, Inflammatory, Neuropathic and Dysfunctional. These are NOT mutually exclusive groups, but can and often occur simultaneously, and all equally important. Let's look at Nociceptive pain for this video.

There are different types of nerves in our body, responsible for different sensations. For example, there is one for pressure and stretch, called mechanoreceptors, one for temperature called thermoreceptors, and one for pain, called nociceptors. Actually in fact, nociceptors are often thermoreceptors as well.

Nociceptive pain is when these nociceptors are stimulated, and activated. Here is my finger. If I bend it, the mechanoreceptors around the joint tells my brain that my finger is being stretched. But it's not painful, yet. If I stretch it more, then the stimulation is large enough to break the threshold of activation of the nociceptors.

So when the nociceptors get stimulated, just like all nerves, they generate electrical signal called Action Potential that gets relayed into the spinal cord, and into the brain. You still will NOT feel any pain however. You'll only feel pain, when your brain, consciously or unconsciously, decides that the signal is important enough for it to be noticed.

This kind of pain, or Nociceptive pain, is the "typical" pain most of us know and understand. Like a joint sprain, a smack on your shoulder, or sudden change in temperature. This sort of pain is important, because it is a warning of a potential threat to our body (3), and absolutely vital for our survival.

References

1. Vardeh D, Mannion RJ, Woolf CJ. Toward a Mechanism-Based Approach to Pain Diagnosis. J Pain. 2016;17(9 Suppl):T50-69.

2. Woolf CJ. Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management. Annals of Internal Medicine. 2004;140:441-51.

3. Melzack R, Katz J. Pain. Wiley Interdiscip Rev Cogn Sci. 2013;4(1):1-15.