Course Notes: Explaining Pain Lorimer Moseley-Style

Why Weren’t you Here??!?!?!?!?!

A late addition to the yearly course list, but a decision I will never regret.


Lorimer Moseley is one of my heroes in the pain science realm and I’ve always wanted to hear him speak. His teaching style—slow paced, humorous, filled with story, and unforgettable—really resonated with me and made his material so easy to understand.

My admiration for him tremendously grew because he was readily admitting if he didn’t know something, critical of his own body of work, and very open to what we we do clinically. I got the impression that he was okay with us practicing how we wish, as long as our treatments are science-informed and coupled with an accurate biological understanding.

I left the talk validated, reinvigorated, and better adept at educating patients. He put on one of the best courses I have been to. If you haven’t seen Moseley live or had the chance to interact with him, please do so.

Let’s go over the big moments.

Sensitization 101

 There are three sensitization types:


  1. Peripheral
  2. Spinal (formerly central sensitization)
  3. Central Sensitization


Let’s break down each.


Peripheral Sensitization

Peripheral sensitization (PS) occurs when primary nociceptors become sensitized. When these nerves fire, they send a danger signal up to the spinal cord in one direction, and release substance P and CGRP in the other direction. The distal discharge equates to neurogenic inflammation.

Primary nociceptors can become sensitized by inputs from the sympathetic nervous system, endocrine system, and immune system.

Adrenosensitivity was a big discussion point this weekend, as it can occur incredibly quickly. When adrenaline is present in the extracellular matrix, adrenoceptors can form in the nerve’s cell wall. We are not exactly sure as to what causes this shift. Not even pain can be implicated. However, genetics do play a role.

Primary nociceptors are sensitive to heat, hydrogen, and mechanical stimuli, so one can diagnose peripheral sensitization via a hot pack.


Spinal Sensitization

Spinal sensitization (SS) is when the spinal nociceptor becomes sensitive. This change was originally called central sensitization, but the literature no longer thinks of this change as such.

Although primary nociceptors can be affected by multiple systems, spinal nociceptors can be sensitized by the immune system only. This is how mirror pains, when a similar pain is produced on the contralateral side, can be created by an immune reaction.

Spinal sensitization only responds to mechanical stimuli, so if a hot pack has no effect you can likely go this direction.

Spinal sensitization can occur without peripheral sensitization. The reverse can only be true for about 30 minutes.


Central Sensitization

Central sensitization (CS) is both increased sensitivity to peripheral input reception and descending facilitation production. Theoretically, any input deemed threatening could be received more readily in this state.


“Threats hide in hard-to-spot places.” ~Lorimer Moseley

Cortical facilitation of relevant neurotags occurs via the following mechanisms:

  1. Brain cells become more easily recruited
  2. Brain cells stay active by inflammatory response.
  3. Adjacent brain cells become active.
  4. Sensitivity of multiple neurotags occurs.


An Order That Would Surprise You

Sensitization, at least to a needle, occurs in the following order


Spontaneous pain for 1-2 minutes (primary nociceptors) → heat sensitivity for 1-2 hours (PS) → dynamic tactile allodynia for 3-4 hours (SS)→ pinprick hyperalgesia for 24 hours (SS)


Then, in a 3-24 hour time period afterwards the contralateral side develops sensitivity—a mirror pain.


Protection System

Sometimes dangerous inputs can lead the brain to produce protective outputs. Pain is one of those possible outputs; a conscious output that can lead to desirable protective behaviors in the short term.

Pain is just one protective system. The system(s) that respond are idiosyncratic. These responses can continually occur, and it becomes harder to produce other outputs when the brain gets so good at playing protective ones. This static replay is a loss of variability, and the longer outputs occur the longer it will take one to recover.

Playing these protective outputs can potentially lead to other problems as well. Take the motor system for example. If a protective motor state is present, secondary problems may arise at other body systems or even other body regions. It’s not that patterns cause pain, but that they leave an individual vulnerable. Hearing this from Moseley was quite validating.


“The strongest neurotags win.” ~ Lorimer Moseley


As great as a threat pain can be, outputs such as fear, thirst, and hunger will usually trump pain. These outputs occur in response to threats greater than potential tissue damage. Comparing pain to these outputs can be enlightening for patients.


Explaining this Stuff

What can be most challenging is explaining pain to patients, but we must give our patients all the possible resources to make the right decisions. Lorimer suggested this occur by the following process:

Challenge a concept → provide an alternative concept → Provide evidence for a new concept


The big concepts we want to hit with our patients include:

  1. Understand pain does not equal injury.
  2. Dethreaten MRIs
  3. Dethreaten the patient’s model.
  4. Provide control.
  5. Teach safe movements
  6. Graded exposure.

Lorimer is big on stories and analogies. I’m sure many of you have heard his stories, but he provided great tidbits to give to patients.


I See

Explaining how vision is analogous to pain is a great way to challenge the concept.

Vision works by light hitting the retina upside-down and brain is able to flip the image so the world appears as it does. However, vision doesn’t always match reality. Take this visual illusion for example.



If you are like most people, you will see a distinct color difference between each block. However, if you put your finger over the border between the blocks you will see they are the same shade. This illusion illustrates how the brain takes a guess at what we are looking at based on many factors, and sometimes it can guess wrong.

Pain works in much of the same fashion. Pain will correct any error it sees from spinal cord inputs via descending inhibition or facilitation.

As vision is our window to the environment, pain is our window to protection. Sometimes that window can be unclear.


Broken Bones

 Pain stops way before a broken bone heals; usually by the time you’re casted. Why?

The need to protect is lost because the cast acts as our protection device, not pain. This analogy is a great way to show patients how pain and tissue healing do not always correlate.


Prized Possessions

 The most vulnerable areas (i.e. brain, spinal cord, pelvis) are reinforced by strong structures covered in nociceptors, like a safe that houses prized possession. This is a built in security system that your body has to protect the goods you possess. Wouldn’t it make sense that anything remotely dangerous happening in that area might set off the alarm cascade?

Watch your patient melt with that explanation.


What Do You Mean by that?

We’ve all had the patient that lists everything medically wrong with them that their doctor told them regarding their pain.

You ever ask them “what do you mean by that?”

You will be amazed at the answers you get. Arthritis is the prime example. A woman I saw the other day mentioned that the doctor said she had arthritis, and I asked her what that meant to her. Her response was classic:


 “I’m not really sure” ~My patient


Unveiling concepts that are unclear to patients can be a huge way to dethreaten scary medical terminology, and turn them around into nonthreatening knowledge nuggets.

Thankfully doctors don’t always explain things well.


Betta Meta’s

How do you guys like the phrases “my bad back” or “my pinky is killing me?” These verbal bits could potentially be components of a threatening neurotag. Keep saying it, and the neurotag persists.

We want to do whatever possible to cease usage of these metaphors. The “bad x” can be dethreatened by clarifying what they mean by that. I like telling patients that their back is so strong that it is putting all the work in to protect them.

The “x is killing me” bit? Getting the patients to realize that the body part is a part of them, and even teaching about the neurotag, can be a great way of stopping this metaphor.


Let’s Emote

Bringing emotion into the mix will help patients learn better. That way individuals can associate a feeling with a concept. I like humor, as does Lorimer. But even sadness, fear, anything can work.

Just pick emotions that an individual will not perseverate on.


Chalk up Your Cues

Lorimer mentioned a study where dentists performing wisdom teeth extraction were told that they were giving placebo pain medication; when in actuality 50% of them were giving actual medicine. They compared this group to a 50-50 split group.

The results?

Even though the practitioners were still blinded, those patients who received the injection from the former group had significantly higher pain levels than those patients who were a part of the latter group.

How is this possible? The answer is in the subtle cues that the practitioners provided. It is these cues that can change the course of a patient encounter.


“We are more compelling if we believe what we believe may work.” ~Lorimer Moseley


Cues beget us to pay greater detail to our patient interactions. Lorimer “got me” on this once was when he was EP’ing me.


Lorimer: “I understand that you injured a tissue and it hurts a lot right?”
Zac: [Nods head fully engaged]

He had me at the nod. When you see an individual nod that shows that you got them, and that is the prime time to start injecting dethreatening knowledge. Whatever words were used to acquire the nod ought to be continually used. These are positive inputs to create positive behavior, and will keep patients agreeable with your education.

Other interesting ways to create evidence-based patient buy-in include:

  • Dressing as attractively as possible.
  • Having visible expensive car keys.
  • Using an extensive vocabulary.
  • Nodding when you want the patient to nod.



  • “I’d like to apologize for the last remnants of snot in my nose.”
  • “When you do research it’s impossible to remove bias.”
  • “Placebo is what we call things we don’t understand.”
  • “We can do some neck mobilizations if you’d like. I just need someone else to teach it.”
  • “If you load someone up on NSAIDS and steroids and shoot a gun behind them they won’t forget it.”
  • “Research doesn’t match the real world.”
  • “We are fearfully and wonderfully complex.”
  • “Pain does not exist until the brain plays the pain tune.”
  • “It’s not the brain that does it, it’s the human that does it.”
  • “We insert ourselves into the brain of everyone we treat.”
  • “Pain is behaving like any other conscious experience.”
  • “Pain is a protector, not an informer.”
  • “If you can reposition them and they’re pain-free. Perfect.”
  • “I believe graded exposure will save 99% of the world’s problems.”
  • “There is no pain threshold. We have a protection threshold.”
  • “Graded exposure is slowly throwing threats into the bucket without creating a protective response.”


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