Michael Reoch, RMT Continuing Education

Two models of what a manual therapist actually does:
The operator model: the therapist finds a problem in the tissue and fixes it. The patient is largely passive. The work is something done to the patient.
The interactor model: the therapist works with the patient and their nervous system. The patient's response to what feels better, what doesn't, and where the comfort is directly guides the treatment. Hands-on work becomes a conversation, and stops being mindless procedure.
Most of us were trained almost entirely in the operator model, even if no one called it that. We learned techniques. We learned to find dysfunction. We learned to correct it.
The interactor model is older than most people think. The late Barrett Dorko was teaching it decades ago. Diane Jacobs built DermoNeuroModulation around it. Pain science has been validating it for 20+ years.
What changes in your practice when you switch frameworks:
Intake conversations get more useful. Pressure decreases. Patient feedback becomes part of the treatment, not a check-in. Outcomes start to depend less on what you know and more on what the patient's nervous system is telling you.
September course works through this in detail on Day 1 and applies it across all four days of lab.
Sept 15–18, Surrey.

Improving the health of Kamloops through family-centred evidence-based registered massage therapy. 4-day DNM continuing education course for RMTs integrating Simple Contact and neurodynamics. Sept 24–27, 2026. Limited to 14 participants.

The most common manual therapy framework most of us were trained on doesn't hold up under scrutiny.
Three examples:
Trigger points — Travell's hypothesis of discrete pathological tissue nodes hasn't survived rigorous review. Quintner and Cohen (Rheumatology, 2015) and others have argued the construct fails on its own internal logic.
Fascial release — Chaudhry et al. (JAOA, 2008) modeled the force required to deform dense connective tissue manually. The numbers exceed what the human hand can produce by a wide margin.
Specific joint manipulation — Ross et al. (Spine, 2004) showed that even experienced clinicians can't reliably target individual segments. The "specificity" of the technique is largely an illusion.

So what's actually happening when our patients feel better?
That's the question Day 1 of the September 4-day intensive opens with. The rest of the course builds a framework that's defensible to your college, your patients, and yourself.
Sept 15–18, Surrey, BC. Link in comments.

Two models of what a manual therapist actually does:
The operator model: the therapist finds a problem in the tissue and fixes it. The patient is largely passive. The work is something done to the patient.
The interactor model: the therapist works with the patient's nervous system. The patient's response to what feels better, what doesn't, and where the comfort is this directly guides the treatment. Hands-on work becomes a conversation.
Most of us were trained almost entirely in the operator model, even if no one called it that. We learned techniques and we learned to find dysfunction. Then we learned this must be corrected.
The interactor model is older than most people think. The late Barrett Dorko was teaching it over 30 years ago. Diane Jacobs built DermoNeuroModulation around it. Pain science has been validating it for 20+ years.
What changes in your practice when you switch frameworks:
Intake conversations continue into the treatment and become more useful. Pressure decreases. Patient feedback becomes an important part of the treatment. Outcomes start to depend less on what you know and more on what the patient's nervous system is telling you.
September course works through this in detail on Day 1 and applies it across all four days of lab.
Sept 15–18, Surrey.

Dates are set. September 15–18, 2026 in Surrey, BC.
A 4-day intensive that integrates DermoNeuroModulation, Simple Contact, and Neurodynamics into one clinical system. 14 RMT seats.
Day 1 opens with what models are outdated in our training (eg trigger points, fascial release, joint subluxations) and why it matters in the room with a patient. The next three days build the framework that replaces it.
Tuition is $995 if registered by June 30.
Link in comments.

New Honest Practice Blueprint episode is out now. This one is an important one although it has its uncomfortable moments.

This one took courage to record.

Bodhi Haraldson — one of the most respected RMTs in BC and former RMTBC research lead — shares his personal journey through a false sexual assault accusation, the legal process, and what came after.

He's talking about it publicly so other RMTs don't have to navigate it blind.

If false accusations or sexual assault are difficult topics for you, please listen with care.

🎙️ New episode live now:
https://open.spotify.com/episode/1E8CrcDMSq7BmZBSbrnYBh?si=wODB1JK0Qv-_MLvBIFxDRg

A quick update on the upcoming DNM 4-Day Intensive.

Spots are starting to fill, and I’ll be keeping the group capped at 14.

If you’ve been thinking about revisiting this material—or learning it for the first time—this is the most updated version of the course.

September 24–27
Vancouver or Kamloops (TBD)

Happy to answer any questions if you're unsure whether it's a good fit.
https://wellandable.ca/services/continuing-education//dermoneuromodulation-dnm-course

If you’ve taken one of my courses before, this will feel familiar—but it’s been updated throughout.

Over the past year, I’ve:

rebuilt the slides
simplified the framework
reorganized the structure
refined the labs and treatment flow

The goal was to make the material clearer and easier to use clinically.

This 4-day format allows more time for:

hands-on practice
clinical reasoning
integrating concepts into treatment

Limited to 14 participants to keep it practical and interactive.

https://wellandable.ca/services/continuing-education//dermoneuromodulation-dnm-course

I’ve been working on this in the background for the past year.

The DermoNeuroModulation (DNM) course is now being offered as a 4-day intensive.

This format brings together:

DNM
Simple Contact
Neurodynamics

into one more integrated system with a clearer clinical flow.

The material has been updated, the slides rebuilt, and the course reorganized to make it easier to apply in practice.

September 24–27 (Thursday–Sunday)
Location: Vancouver or Kamloops (TBD)
Limited to 14 participants

Registration is now open.

https://wellandable.ca/services/continuing-education//dermoneuromodulation-dnm-course

I read the recent PainScience post “Pain needs nociception” and wanted to share my genuinely mixed reaction.

First, credit where it’s due: the post usefully pushes back on the occasional over-enthusiastic shorthand that pain is “just brain-made.” That framing does drift into non-biological territory if we’re not careful, and the Weisman, Quintner & Cohen paper raises a legitimate conceptual challenge to how loosely we sometimes repeat aphorisms like “nociception is neither necessary nor sufficient for pain.” Fair point.

Where I start to squint (and re-read definitions, which is usually a sign I’ve wandered into a terminology problem rather than a data problem) is around how nociception is being used. Under standard IASP definitions, nociception refers to neural encoding of actual or threatened tissue damage, initiated at peripheral nociceptors. Broadening that term to include any neural activity involved in pain makes the statement “pain always requires nociception” hard to disagree with — but also a bit tautological, and less helpful mechanistically.

This is where I think the blog slightly overreaches by implying that papers describing pain without ongoing peripheral nociceptive input are simply false. Many of those papers aren’t denying biology or neural necessity — they’re describing altered central processing, which (last time I checked… and I check often because I worry I’ve missed a memo) is still well within mainstream pain science.

The broader literature still seems fairly consistent on a few points:

Pain ≠ nociception (IASP, 2020)

Central sensitization and nociplastic pain describe real, measurable phenomena, even if their boundaries remain fuzzy (Nijs et al.; Kosek et al.)

The Weisman et al. paper is a thoughtful conceptual critique — but not the final word on pain mechanisms (as tempting as it is to treat Brain papers that way…)

Relevant reading for anyone interested (and for me, again):

IASP Pain Terminology & Definition (2020)

Nijs et al., Pain — central sensitization & nociplastic pain

Kosek et al., Pain — strengths and limitations of nociplastic pain

Weisman, Quintner & Cohen, Brain (2025)

Bottom line (from someone who spends too much time worrying about words): the blog is a useful corrective against extremes, but I don’t think it “closes the case.” This still feels like a definitional and conceptual debate more than a refutation of existing evidence.

Happy to be corrected — preferably gently, preferably with citations.
https://www.painscience.com/blog/pain-needs-nociception.html?fbclid=IwY2xjawOv8JlleHRuA2FlbQIxMABzcnRjBmFwcF9pZBAyMjIwMzkxNzg4MjAwODkyAAEe7Ervgs_fwnoUVgc9YMCHVqX6pGqMKXQVeoHsqRlyI-fRUbXt6B-4OGd48-I_aem_WIPoM8Gc1FLVaKLF5d841A

Pain needs nociception: 3 new papers The brain cannot create pain; there has to be something wrong in the body. But what?