Did you miss Movement Debrief live yesterday? Though much more fun live, I have a video of what we discussed below.
This debrief was quite fun, as we had an impromptu viewer q&a. Thank you Alan Luzietti for the awesome questions! If you follow along live on Facebook or Youtube, I will do my best to answer any questions you ask.
Yesterday we discussed the following topics:
Why you should emphasize sagittal plane activities longer than you think
How to coach exercises to maximize client learning and compliance
Why detaching from your client encounters makes you a better clinician
Viewer Q&A – “centering from the chaos” & TFL Inhibition
Lastly, if you want the acute:chronic workload calculator I spoke about, click here.
You shed that mindset with the game on the line. You must do all in your power to get that player back on the court tonight, expediting the return process to the nth degree.
I had a problem.
Figuring out the most efficient way to treat an ankle sprain was needed to help our team succeed. I searched the literature, therapeutic outskirts, and tinkered in order to devise an effective protocol.
The result? We had 12 ankle sprains this past season. After performing the protocol, eight were able to return and finish out the game. Out of the remaining four, three returned to full play in two days. The last guy? He was released two days after his last game.
It’s a tough business.
The best part was we had no re-sprains. An impressive feat considering the 80% recurrence rate¹. Caveats aside, treating acute injuries with an aggressive mindset can be immensely effective.
Note from Zac: This is my first guest post, and to start things up is the one and only Trevor Rappa. Trevor was my intern for the past 9 weeks and he absolutely killed it. Here is his story.
It’s very exciting for me to get to write a guest post for Zac’s blog that I have read so many times and learned so much from. The experience I have had with him over these past 9 weeks has been incredible and I hope to share some of it with all of you that read this.
He challenged me to think critically in every aspect of patient interaction: how I first greet them, which side of them I sit on, the words I use, and how I explain to the patient why I chose the exercises they’ll go home with. All of this was to create a non-threatening environment to help to patient achieve the best results they can.
He also taught me how to educate patients with a TNE approach, incorporate other interventions such as mirror therapy into a PRI based treatment model, and deepened my understanding of the neurologic concepts behind performance.
Therapeutic Neuroscience Education
Perception of threat can lead to a painful experience which will cause a change in behavior. It’s the PT’s role to introduce a salient stimulus to attenuate the perception of threat in order to cause a positive change in experience and behavior (Zac and I came up with that, I really like it).
Pain is not the enemy. Teaching patients that their pain is normal and it doesn’t always mean that they are damaging themselves can be challenging as pain is often the reason patients seek out or are referred to PT. Some of the points we tried to teach patients were
Pain is there to keep you safe, which is good
Pain does not equal tissue injury
No pain, no gain is not what we’re looking for
Discomfort is okay
Knock on the door of pain, don’t try to kick it down
A large part of educating patients is helping them re-conceptualize why they are having pain. Most patients think of pain in terms of a pathoanatomical model (ie tissue abnormality=pain) and this is perpetuated by a lot of members in the medical community. The pathoanatomical language often causes a higher perception of threat and induces greater feelings of being broken, hopeless, and unfixable.
Re-educating the patients that what they are experiencing is normal and teaching them why it is normal helps decrease their perception of threat. We do not want to use language that will make patients more threatened, like telling a 20 year old that they have the spine of an 80 year old (numerous times our patients have been told that by other medical professionals). Getting them out of a mindset that if they move a “faulty tissue” they will make their situation worse is one step in this process.
Regardless of whether the patient is dealing with a more acute injury or one that has become chronic, there are three things we taught each patient that we would do in PT to help decrease some of the sensitivity they may be dealing with. Those three things are movement, space, and blood flow. These three things require the patient to be active in their therapy which gives them control.
Many of the patients with chronic conditions had stopped doing the things they enjoyed. Giving them activities which they can do without perceiving pain, or that can help decrease their pain, shows patients that they do not need to rely on external passive interventions to feel better. Getting patients to believe/understand that they have the control and power to make themselves feel better is one of the most important things a PT can do.
Mirror therapy, sensory discrimination, and PRI
Learning how to use different interventions to help decrease sensitivity and pain was huge for me. We used mirror therapy with different types of patients whether they had chronic pain or were post-surgical. The mirror activities usually started with the patient moving their unaffected limb while watching their affected limb move in the mirror. For example, if you right arm hurts you’d move your left arm while looking at the mirror because it would appear that your right arm is moving. We would progress patients to where they were moving their affected limb behind the mirror while still watching the reflection of their unaffected limb moving in front of the mirror. With the example above, you would still be watching the reflection of your left arm in the mirror making it look like your right arm is moving but would also be moving your right arm behind the mirror. This helped introduce patients to moving a sensitive area without experiencing pain, thus decreasing the threat of movement.
Another intervention I had not used before was sensory discrimination. We used this mostly in our post-surgical or more acute population to help decrease the local sensitivity after an injury and to try de-smudgify (that may or may not be an actual word) their homunculus [note from Zac: Totally is].
Sharp-dull discrimination was used first, then we progressed to two-point discrimination and usually ended with graphesthesia. The progress for patients from not being able to discriminate between sharp-dull to having graphesthesia showed me how powerful the role of the somatosensory homunculus is in the pain experience.
And of course, I learned more PRI from Zac. He challenged me to use more integrated non-manual techniques with patients while also limiting the number of cues I used. This was great because it is very easy for me to over coach these techniques. He also gave me a better understanding of some of the big concepts in PRI, such as neutrality.
Neutrality vs Hypofrontality
Neutral is a huge word in PRI that is often thought of as the end game when in reality it is just the beginning of a PRI treatment. The end goal is to get someone alternating and reciprocal. The idea of neutral always made sense to me as a good goal for performance as “neutral” joint positions is where the greatest force would be able to be produced. Talking to Zac about this he brought up what Bill Hartman Grandpa 🙂 has said: Neutral is a neurologically prefrontal state in which learning can occur, as the prefrontal cortex (PFC) is active during tasks that require attention. However, this is not a state you want an athlete performing in.
An active PFC is good when athletes or patients are in rehab because their cerebellum and basal ganglia are learning new movements that can then be used with less activity from higher cortical areas during performance. The movements used during these activities can become reactive after enough learning, practice, and repetition (those 3 things go hand in hand).
During performance or training we would not want an athlete using the higher cortical areas that elicit attention as this would make them slow and inefficient. Instead, we would want them fast and efficient (ie reactive and reflexive). A transient state of hypofrontality allows an athlete to reach a state of “flow”, which Mihaly Csikszentmihalyi describes in his book Flow, which is where the highest levels of performance occurs. This would allow the lower reactive (cerebellum and basal ganglia) and reflexive (brain stem) centers of the brain to essentially take over making them fast and efficient.
So from a theoretical neurologic stand point you do not want an athlete in a prefrontal state during performance. Good rehab and programming can help them become alternating and reciprocal through graded exposure and relearning of certain movement patterns in a neutral (prefrontal) neurologic state. Once this foundation is there, power and capacity can be added through training (which Zac talks more about here ). This may allow an athlete to stay alternating and reciprocal during transient states of hypofrontality when performing, not “neutral”.
Another concept that stood out to me from talking with Zac is the difference between extensor tone and extension. Extensor tone is necessary for power production during performance but it does not necessarily mean that the athlete is going into a position of extension. When someone is in extension they limit their degrees of freedom for movement and thus their movement variability. Using extensor tone from a neutral position, for lack of a better term, would allow them to display power while maintaining their potential movement variability (be alternating and reciprocal). This idea was something that made things click for me.
I learned a lot from Zac and want to thank him for all his help and time he spent teaching me. Needless to say, this was an amazing clinical internship for me and I cannot recommend enough that other students should try to get Zac as their CI or for patients to get treated by Zac. He is the real.
And now what everyone has been waiting for… Zac quotes
Help for cueing exercises
“Shakin’ like a polaroid picture”
“We don’t want Fat Joe and the lean back”
“Do you remember the three little pigs? I want you to be the big bad wolf and blow their house down”
“Do you have the big 3? Jordan (L abs), Pippen (L adductor), and Rodman (L glute med)?”
“We like a tight right butt and we cannot lie, the other therapists can’t deny”
“I’ll start calling him Buffalo Bill, cause he’s abducting like crazy”
“We don’t want you to have hamstrings like Goldmember”
Zac after getting his wisdom teeth out, he doesn’t remember saying these things
“I have lateral trusion!”
“Check out this IR” and then he self-tested his own HG IR
“I ain’t got time to bleed”
“Nobody makes me bleed my own blood”
“If you ain’t assesin’ you guessin’”
“There’s 45 miles of nerves in the human body if you put them all in a straight line, but don’t try it at home cause you’ll die.”
“…hmm..interesting” in Bill Hartman Grandpa’s voice
“…sure about that?” in grandpa’s voice
“Her teeth told me she had bunions”
“I don’t know why he told us the same diagnosis five times.”
“Breathing is really important. The research has shown if you don’t do it you will die”
“How about this word, variability. How about this word, salience. How about this word, anti-fragile. How about this word, POTS.”
We are hosting several courses at my clinic this year, and we would love to have you, the readers, attend.
The three courses that East Valley Spine and Sports will be hosting are all excellent courses. I have taken two of these classes prior, and the third I have taken a prior rendition of. And let me tell you, these courses are boss.
Aside from us bringing some excellent content, you will also have the opportunity to hang out with a good group of people, and imbibe in some good beverages with me.
Here is what we are bringing.
PRI Pelvis Restoration: March 28th-29th
I took this course a little over a year ago (read the review here) and I am very excited to be learning from Lori again. She presents this very complex material in a systematic and understandable fashion.
ISPI Neurodynamics: The Bodies Living Alarm: October 17th-18th
I took a version of this class when Adriaan spoke for the NOI group, and I am excited to see what tweaks have been made since. This time we are bring Louie Puentedura in to teach the class. I am excited to hear his perspective, as I have never seen him talk. Adriaan speaks highly of him, so he’s okay in my book!
You can be amazed at what the patient can actually be do at this stage to expedite the rehab process once movement constraints are lifted.
The most common upper quadrant restriction involves no movement of the involved extremity.
The goals during this stage ought to include:
Promote a safe healing environment – reduce fear, pain, swelling, etc.
Restore local mobility
Restore system variability
Remap affected regions in the somatosensory homunculus
Challenge the aerobic system
Let’s take a patient I am seeing post-rotator cuff repair on his right arm. He cannot move his arm for 6 weeks.
Top priority of course is restoring range of motion, so session bulk was spent on pain-free manual therapy and passive range of motion. For home he gets elbow/wrist ROM and nerve glides.
But there is no way in hell I am doing that for 60 minutes.
There are many other things that this fellow can work on aside from basic range. Let’s address the other qualities.
Restore System Variability
In PRI-land, this gentleman was a PEC/RBC/RTMCC. We began to address this protective pattern day 1 after surgery.
Reduce sympathetic tone, reduce threat perception, promote a safe healing environment. Everybody is happy.
Since I knew he would be living in a recliner for the forseeable future, we kept things simple by blowing up a balloon.
One week later our guy came in as a LAIC/RBC with decreased left hip internal rotation, so we shifted our emphasis towards improving right apical expansion while shifting into his left hip.
With this strategy, we were able to maximize system variability within the confines of his restrictions. Gaining apical expansion on the right side was a nice way for the patient to relax the shoulder tissues while keeping the repair intact.
Remap Affected Regions
Use it or lose it reigns king in post-op land. But how can we get this gentleman to use his arm while respecting the passive-only barrier?
Here is where I love graded motor imagery the most. The shoulder’s motor pathways can still run while the repair stays intact.
He ended up blowing this stage out of the park, so once we went through all the different challenges this program allows we went straight to explicit motor imagery.
I asked our guy to visualize what his shoulder looked like without the brace first. Once he was able to do this, I had him imagine moving his arm in various movement planes, to progress to envisioning ADL performance with his affected extremity.
In the clinic, I would teach him push/pull movement on his left arm while he imagined performing those actions on his right.
Once he mastered imagery, we began to implement mirror box therapy.
We first started out by just watching him move his “right” arm in the mirror, which he said was very freaky.
Despite the freakiness, it blew him away how much this technique reduced his pain and stiffness.
Once he could do basic movements no problem, we had him work on push/pull movements using his left hand while watching his “right”arm.
His most challenging piece? Open loop arm movements. This task was a beast for his mind:
Combining GMI with working the non-affected extremity tremendously expedited re-learning basic movements on his affected extremity as we progressed later into postoperative care.
Challenge the Aerobic System
Our guy is in his 50’s and a blue collar worker, so we aren’t getting super wild and crazy here.
Day one we emphasized nice easy walking 20-30 minutes per day to increase circulation and promote healing.
Clinic-wise, we taught him squatting, deadlifting, pressing, and rowing. To emphasize the aerobic system, we kept things at tempo pace to emphasize slow-twitch hypertrophy and aerobic development.
2-4 sets of 10-12 reps
Pace 3 second eccentric—no pause—3 second concentric. I tell patients to say this mantra slowly – Screw…you…Zac (eccentric) Screw…you…Zac (concentric). This mantra also helps boost the immune system because patients find it funny. Two points for me!
30-40 seconds rests between sets.
Later Rehab Stages
The later rehab stages look somewhat similar to typical fare, though I do not emphasize isolated strengthening so much.
Once the active assist/active unresisted phase is allowed, we switch to that stuff. Shoulder remapping becomes a greater active process, so most of GMI is stopped. Let’s get him moving.
Our program also shifts toward him using his right extremity to aide in variability restoration. He has limited flexion, so I like a doorway lat stretch:
[side note: amazing that most comments I’ve heard on this vid involve my glutes and not the technique. Upon reflection of most of my life, this probably is not as surprising]
I also like him doing unresisted reaching:
We still emphasize challenging the aerobic system and the unaffected extremities, but this usually accounts for about 20% of the session at this time.
Once we can start resistance training the extremity, we keep things simple. I like push/pull movements and static/dynamic motor control exercises. So we teach our guys armbars, get-ups, carries, crawling, etc.
I don’t use a whole lot of isolated cuff work during the rehab process. The cuff doesn’t really work as a prime mover, so unless the goal is cuff hypertrophy (aka gettin’ Swolebodan Milosevic), I don’t do it.
In the cases that I have scrapped cuff isolation exercises, I still saw manual muscle testing improve just the same. So let’s teach the cuff to be a cuff.
We finish the rehab process by making it look a lot more like fitness. By the end, the hope is to have system variability restored, local mobility in the clear, and strength up to snuff. Teach your guys and gals the basic movements and emphasize patient-specific functional activities, and you are in the clear.
That’s where I am right now with upper quadrant post-operative care. There is a lot that these folks can be doing, and my challenge to you is to make those early stages of rehab some of the most exciting for the patient.
My gluttony for punishment continues. This time, I had the pleasure of learning Diane Jacobs’ manual therapy approach called Dermoneuromodulation (DNM).
My travels took me to Entropy Physiotherapy and Wellness in the Windy City. These folks were arguably the best course hosts I have ever had. We had lunch!!!! Both days!!!!! That is unheard of, so a big thanks to Sandy and Sarah for putting the course together.
I took DNM out of curiosity. I have been lurking around Somasimple on and off for the past couple years, and wanted to learn more about the methods championed there.
Believe it or not, I have yet to take a pure manual therapy course, DNM seemed like a great way to get my hands dirty. That darn PRI has lessened the hand representation in my somatosensory homunculus!
One reason I haven’t taken a manual course is due to the explanatory models many classes are presenting. It seems as though few are approaching things with a neurological mindset, but I was pleased to hear Diane’s model. It is the best explanation I have heard yet.
I know that I usually list my favorite quotes at the end of the blog, but I wanted to share the best quote of the weekend right off the bat:
“I don’t know why.”
I heard this phrase so much throughout the course and it was quite refreshing. Diane made few claims about her technique, admitted who she “stole” from, and embraced the uncertainty that goes along with how her technique works.
Diane didn’t advertise her method as the end-all-be-all, and encouraged all of us to make up techniques of our own. She is just offering a non-painful sensory input that works quickly.
I wish more courses were this way.
Let us now press onward to a fantastic explanation for manual therapy.
Manual Therapy – An Interaction Between Two Nervous Systems
Diane started off with manual therapy’s theoretical basis. Manual therapy works predominately through your nervous system. We are made up of a brain, spinal cord, and nerves that extend from the cord.
The brain can be simply broken up into two components: the human brain and critter brain. The human brain sits our higher activity centers, and the critter brain runs the processes that keep us alive.
Under threat, the critter brain is going to do everything in its power to keep us alive, and this change can involve the protective mechanisms that go along with pain.
The critter brain carries out its processes through the body’s nerves. Nerves in the body tell the brain what’s going on, and the brain then tells nerves how to respond.
In order to calm our critter brain down, the clinician can communicate with the nervous system through cutaneous nerves. Our goal with our interventions is to touch the patient without hurting them. Hurt could irritate the critter brain. Instead, we want an enjoyable context for touch.
The patient’s role…Wait, what???!!!
Yes, the patient’s role in the manual therapy process is to guide the clinician to what feels best. It is this interactive and interoceptive model that helps reduce threat perception. This context allows for the patient to be a little more in control of the manual therapy process.
It Rubs the Lotion on Its Skin
The skin is a pretty cool organ that can hold 20% of our blood supply and maintain temperature homeostasis. It has both peripheral (PNS) and central (CNS) nervous system influences. The PNS automatically activates to maintain skin temperature and the CNS can express itself through the skin. Those times in which you are embarrassed or scared reflect CNS status through your skin.
Due to the skin’s high innervation and vascularity, anytime we touch the skin we affect the neurovascular array. This change occurs through facilitating mechanoreceptors and physically altering cutaneous rami position. The nervous system then evaluates this information to determine if the touch is a threat or not.
Tissue information is received through receptors. There are tons of them, but we have a few major players:
Rapidly adapting mechanoreceptors – Turns on and shuts off by itself
Thermoreceptors – Responds to temperature change for duration of stimulus.
Nociceptors – Responds for stimulus duration. Can be set off by going perpendicular on skin.
Pacinian corpuscles – Turns on with stimulus onset and removal. Will continuously fire if stimulus fluctuates.
Meissner’s corpuscle – Turns on with stimulus onset and removal
Ruffini endings – respond to lateral skin stretch and are non-nociceptive. Slow adaptors to stimulus. Can fool the brain to alter muscle tone with skin stretch.
Merkel cells – slow adapting to stimulus.
All the above receptors respond to stimuli and communicate information to the brain along sensory nerves. It turns out sensory nerves are incredibly long. Many of these nerves go directly from the skin to the brain. One cell! Anytime you touch the skin you are touching a direct extension of the brain.
Sensory input travels via the mechanoreceptors through the dorsal columns and spinothalamic tract in the spinal cord. Interestingly enough, the spinothalamic tract does not only carry nociception, temperature, and crude touch. Pleasant touch can also travel along this pathway.
The Dorsal columns input goes to the thalamus, which sends information to the somatosensory cortex. The spinothalamic tract goes to the thalamus first as well, followed by the somatosensory cortex, anterior cingulate cortex, and the insular cortex. These three areas are what Diane noted as “threat evaluation areas.” These areas are part of your critter brain.
Once the brain receives this information, it essentially talks to itself to determine if this information is important or not. If important, an output occurs to respond to the input.
Many brain areas are a part of this conversation. The following locations contribute to the desired output in a particular way:
Anterior cingulate cortex – bridge between instinct and rational; makes us worry about pain.
Orbitofrontal cortex – defers, suppresses, differentiates touch, interprets emotions (if you are in a bad mood, this is how your patient will know it…so be happy!).
Dorsolateral prefrontal cortex – Chooses behavior. This area is where therapeutic neuroscience education targets.
Pain is one possible output in response to various inputs. If pain is the desired output, changes can occur to increase sensitivity.
One possibility is hyperalgesia, in which noxious stimuli becomes extra sensitive. Hyperalgesia can be primary or secondary.
To understand the two, we should first look at a sensory neuron.
A sensory neuron has two ends. The end that connects to the tissue is the terminal pole, and the end that travels to the spinal cord is the central pole.
Primary hyperalgesia affects the terminal pole. Substances released by injured tissue activate nociceptors at this pole, creating the information cascade sent to the brain described previously. We also know this as inflammation.
As the inflammatory process progresses, nociceptors send substances out to the tissues to promote enhanced firing. This change creates peripheral sensitivity, and is normal.
Secondary hyperalgesia (aka central sensitivity) has more fun at the central pole. TRPv1 is a receptor at the central pole that increases spinal cord and blood-brain barrier permeability, which allows for more nociceptive transmission to be received. Serotonin can descend from the brain to the spinal cord and sensitize these receptors as well.
Other changes that occur in secondary hyperalgesia include glial and satellite cells lowering the threshold at which nociceptors fire. The name of the game is to increase the nociceptive information coming in.
Both of these algesic mechanisms can simultaneously occur to protect a potentially compromised area. However, pain may not necessarily be experienced. Nociception involves threat detection, whereas pain involves threat perception. The two are not equal entities.
“The labeling of nociceptors as pain fibres was not an admirable simplification but an unfortunate trivialization.” ~Patrick Wall
Nerves n’ Stuff
The neurovascular bundle is connected via regional feeder vessels. These vessels ought to slide and glide with the nerves so blood supply is maintained. Movement is what keeps this system healthy.
These connections are vulnerable and can become sensitive to mechanical deformation. Too much or not enough movement can decrease the nerve’s oxygen and glucose supply. A nerve will let you know if it does not get fed.
Deformation could translate into neuropathic pain, which is defined as pain caused by a lesion or disease in the somatosensory system. Neuropathic pain is not a diagnosis, but a descriptor.
The way one could determine if neuropathic pain contributes to one’s complaint is done quite algorithmically. The following must be present:
Leading complaint must be pain.
Pain distribution must be neuroanatomically plausible.
History should suggest relevant lesion or disease.
Negative or positive sensory signs contained to lesioned area in question.
Diagnostic testing confirming lesion or disease explaining neuropathic pain.
The fewer of these criteria positive, the less chance there is of having neuropathic pain.
Theory into Therapy
Diane stressed that a therapeutic context must be established before implementing a manual intervention. This foundation occurs via a 4-step process
Listen – Allows the patient to map you in their story. Your listening models how they listen to themselves.
Interact – Explain pain. This part will plant seeds to regulate future stressors.
Treat – Provide non-nociceptive therapy, making sure to give the patient locus of control.
Wait – Do not correct; wait for physiology to change and the desired output to emerge.
The object is to create the largest amount of descending modulation possible. We therefore mobilize the cutaneous nerves via “yesiceptive” contact and interaction.
Though Diane does not believe in trigger points, she does believe in sore spots that often have a different feel about them. Our goal is to change these sore spots without worsening them.
Cutaneous nerves anastomose in various ways, so everyone’s anatomy is going to be slightly different. Thus, there can be no precision or specificity with treatment. We just have to somehow move nerves in a fashion that results in reduced pain.
The assessment process was my one gripe with the course. Each technique was given clinical situations that they may work with. We then assessed with active movement followed by palpating tender spots. However, these spots can be present on many people even if pain is relieved, are unreliable to assess, and do not always contribute to the patient’s complaint. How can we say that performing this intervention is the right thing to do for this patient?
Well Diane freely admitted palpation’s unreliability, she has also been practicing long enough that she has the pattern recognition to know when techniques ought to be implemented. Novice clinicians likely lack this skill. There must be some way to provide an assessment that may lead you to performing one mobilization compared to another.
I espouse Charlie Weingroff’s principle of “can your treatment beat my tests.” Since I am a PRI enthusiast, I used those objective measures to test treatment efficacy. When implemented thoughtfully, DNM can change PRI objective measures fairly quickly and in a pain-free manner.
Zac = sold on both counts.
DNM is actually fairly simple to perform. The technique is a combination of positional release with skin stretch; fine-tuning performed throughout to maximize treatment effect.
Diane gave us many techniques that seem to work over specific areas, but really you can stretch skin in any fashion. Here are some examples of the basic techniques utilized in the course.
Longitudinal distraction – Nerves move up.
Shearing distraction – Nerves are lifted and twisted.
Unloading – Nerves move up.
Contralateral unloading (the balloon) – Go to the opposite side of the sore spot.
Once these techniques are implemented and symptoms change; exercise ought be to given to reinforce the changes. Though no specifics were given, Diane suggested ideas of using positioning strategies, taping, self-DNM, etc. Her objective was to give us the manual technique, then supplement with our exercise strategies of choice.
Overall I really enjoyed Diane’s course. She has given the best manual therapy theoretical explanation I have heard, and the technique is very gentle and effective. She can beat my tests. I think that if these maneuvers are implemented into a sound assessment, you can add a very powerful sensory input to your repertoire.
Verdict: Do it. The neuroscience alone is worth the price of admission.
Nerves slide and glide like a telescope.
A rete is a dense convoluted birds nest of cutaneous nerves over a bony prominence. These are over most every bony prominence.
Dianetics (See what I did there??)
“We belong to our brain more than our brain belongs to us.”
“We’re not treating anatomy, we’re treating physiology.”
“Spinal cords have not got much smarter since fish days.”
“You can’t trust the brain pretty well. It makes up stories.”
“It’s never a good idea to treat someone who is feeling better than you are.”
“Therapeutic neuroscience education is accurate and relevant pain information.”
“Pain is physiological.”
“You are only as old as your C-fibers.”
“It probably serves us well to not believe everything our brain tells us. “
“Pain is the story built from all inputs.”
“Pain descriptors are more of a way for the patient to export their feelings.”
“Having a license to touch people is an enormous privilege.”
“I can’t think of a better thing then using human brains to help other brains.”
“The less you do the better results you are going to get.”
“I have to tell you up front. I am a trigger point atheist.”
“Evolution is weird, and it’s not that smart actually.”
“When I don’t have a monitoring hand I’ll use my head to push the skin on the butt. I call it the head butt technique.”
“There will be asymmetric positions people adopt. It’s their comfort position.”
“We’re asymmetric in our behavior.”
“We’re not going to deal with your ovary by the way.”
“Those who have IT band syndrome, I don’t even know what that means.”
“I found this on the internet so it must be true.”
“The pelvic floor holds up a bunch of stuff. And you don’t know what you’ve got ‘til its gone.”
“Heels just love to be cranked on.”
“Let your brain be creative when you treat.”
“It’s [DNM] soft and easy so you can die comfortably at your job.”
You may have noticed that my blogging frequency has been a little slower than the usual, and I would like to apologize for that. I am in the midst of creating my first course that I am presenting to my coworkers. It has been a very exciting yet time-consuming process. It makes me excited and more motivated to someday start teaching more on the reg.
Ever since I started blogging people started asking me questions. These range from many topics regarding physical therapy, career advice, and the like. Some of the more frequent ones include:
What courses should I look at?
Any advice for a new grad?
Seriously, Bane. What’s the deal?
But the one I get asked more often then not is as follows:
“Zac, how do you integrate PRI into a pain science model?”
A great question indeed, especially to those who are relatively unfamiliar with PRI. With all the HG, GH, AF, FA, and FU’s, it’s easy to get lost in the anatomical explanations.
Hell, the company even has the word (gasp) “posture” in the title. Surely they cannot think that posture and pain are correlated.
I think there is a lot of misinformation regarding PRI’s methodology and framework. What needs to be understood is that PRI is a systematic, biopsychosocial approach that predominately (though not exclusively) deals with the autonomic nervous system. The ANS is very much linked into pain states, though not a causative factor.
But of course, that may not be enough. Perhaps we can dig a little deeper into what may be going on. My hope with this blog is to make a guide to integrating two very effective paradigms which I feel are not mutually exclusive.
PRI Patterns and Nociception
David Butler discusses many nociceptive processes, including mechanically-induced pain, inflammation, and ischemia.
I feel that the PRI patterns, albeit normal, could contribute to nociceptive processes. Mechanical pain makes the most sense. We could think of this process as typical anatomy/biomechanics. If one is in a right-lateralized and extended position, certain areas are going to be more prone to mechanical deformation than others.
Inflammatory processes could be caused by acute injuries secondary to position. The easiest example I could give would be an ankle sprain. If someone is in a right lateralized pattern (a la Left AIC), the right ankle/foot complex would be more supinated, thus being more at risk to sustain an ankle sprain. So in these cases, a right lateralized pattern could be one of many risk factors for leading to an injury.
Ischemic nociception is where things get interesting. There are two ischemic features that Butler mentions in “The Sensitive Nervous System” that stood out to me:
Symptoms after prolonged or unusual postures.
Rapid ease of symptoms after a change of posture.
If I am right lateralized and unable to leave right stance, this position could become ischemic after a prolonged period. Less movement, less axoplamsic activity, less blood flow.
Moreover, symptoms would be much more challenging to relieve. If I am unable to adduct and internally rotate my hip maximally, then I effectively limit what movement planes I am capable of utilizing. This concept is what Bill Hartman calls movement variability. When a position becomes nociceptive, movement must occur to reduce danger signals and restore axoplasmic and blood flow. I am looking for freedom. But triplanar activity is unachievable, movement freedom becomes a limited resource.
I simply lose the ability to change posture, which limits my ability to relieve ischemia.
PRI Patterns and Peripheral Neuropathic Pain
When I am in right or left stance, the nervous system slides and glides to accommodate position. Suppose I am in right stance. Right stance would require my right hip to be more extended, adducted, and internally rotated. My left hip would be flexed, abducted, and externally rotated.
When my hips are positioned as above, the sciatic nerve would be more taut on the right and slacked on the left. Now if I never leave right stance (aka left AIC), then I could potentially be more at risk for tension impairments on the right.
Another example would involve spinal position. Research demonstrates that humans have a naturally right oriented spine (here & here) which is precisely what PRI advocates. This orientation may bias more compression on the right nerve root than the left. If we have someone who presents with a dominant PEC i.e. spinal hyperextension, we could potentially see increased compression bilaterally.
PRI, What a Great Defense
Now of course, we know very well that nociception and peripheral neuropathic issues are neither necessary nor sufficient for a pain experience. So how does PRI relate to pain?
Simple, the PRI patterns are the perfect protective postures for us to assume when we are threatened.
We drive these patterns via our autonomic nervous system. If you read Stephen Porges work, he discusses the concept of neuroception. Neuroception is how our nervous system’s evaluates risk. We take all sensory information in regarding our environment and determine if we should fight, flight, freeze, or relax and socialize.
When we neurocept (is that a word??) something as a threat, we will become more sympathetically driven and likely use our most efficient processes to respond to the threat. We use what we know.
We bias ourselves to the right because motor planning occurs in the left hemisphere regardless of hand-dominance. If I stand on my right leg, I simply am better able to make my next move than if I were to stand on my left.
Breathing will become faster and shallower. Take a look at the diaphragm. Which side is larger?
The right hemidiaphragm is larger and more powerful than the left. If I am already biased to the right and have a stronger muscle on the right, breathing becomes a less conscious process.
My point of listing these plausible changes in response to theat is to demonstrate that we are fairly similar creatures. Bill again, helped me realize this on a post he made at Somasimple.
If a lion were to walk in the room, what physiological changes would we undergo? Our heart rate would increase, pupils would dilate, HRV decreases, we sweat, etc. Are these responses not the same for all humans? These physiological changes are a common human pattern. Could it be possible there is a common threat response in postural and muscular activity as well? This pattern of positioning and neurological bias is what I feel PRI has put together more completely than anyone else.
Granted, we can still account for individual differences, but realize these changes are likely minor variations off the normal response.
When under threat, your heart rate increases 20 beats per minute, mine increases 10.
When under threat, your sweat accumulates on your brow, mine on my palms.
When under threat, your left anterior hip capsule becomes lax via compensatory external rotation, mine stays intact after compensatory external rotation.
The positions utilized are the farthest removed from the typical protective response when we perceive threat. If right stance with increased extension is what we do when we are threatened, then I am going to get you into left stance and flex you until the cows come home.
PRI essentially is graded exposure into left stance and parasympathetic paradise.
That doesn’t mean that PRI is going to eliminate the entire pain experience in all cases. There are some people who have injuries that are producing nociception, and may take time to heal. There are some people who have enough neural sensitivity requiring a hands-on or neurodynamic approach. There are some people who have centrally-maintained pain experience that requires graded exposure, pacing, and homuncular refreshments. The autonomic protective response is one piece of the puzzle, and altering that piece is the only way one can know if it is contributing to one’s complaint.
Therapeutic Neuroscience Education…PRI Style
So usually when I educate patients I just run through the above as quickly as possible…
Okay that’s not 100% true.
I actually use the concept of a home security system to explain how PRI patterns are a part of the pain experience. Go ahead, watch the video, I’ll wait.
So as you can see, I do not go into nitty gritty detail of PRI methodology. It is mostly not necessary and could potentially increase threat perception. But framing the system as done above can help the patient understand why we may work at areas far away from the pain experience. We are treating what area of the system continues driving the protective response. We are treating the person.
PRI is a very powerful system that does not have to go against current pain research, not that it ever did. But the above may be a potential framework and justification as to how PRI affects the pain experience. It is the framework that I operate on, and will continue operating on until I am shown otherwise.
How’s Your Pain How’s Your Pain How’s Your Pain How’s Your Pain?
To purge onward with developing some semblance of chronic pain mastery (ha), my employer had the pleasure of hosting a mentor and good friend Adriaan Louw.
I first heard Adriaan speak in 2010 when I was in PT school. I was amazed at his speaking prowess and the subject matter. Unfortunately, my class could only stay for a little while in his course, and onward life went.
I went on with my career focusing on structure and biomechanics and forgetting about pain. It wasn’t until I ran into Adriaan again two years later. He was teaching me Explain Pain (EP), and forever changed how I approached patient care.
A lot has changed in two years. EP and TNE are quite different courses, and I learned so much this weekend that I continue to become more engrossed with what I do.
So thank you, Adriaan, for playing a huge role shaping me into who I am today. I have now become very much more interested in what ISPI has to offer, and I think you should too. And no worries Adriaan, I will stay hungry 🙂
So without further ado, here is what I learned.
The Power of Words
It’s getting worse. One person out of 3.5 has chronic pain. Many of these people have tried many treatments, heard many explanations, and lost all hope.
And here they are, in your office. The patient thinks you are going to be another statistic. Another failure. Another person who can’t help them.
So what do you do?
The answer: Apologize, and tell them they are going to be okay.
These are some of the most powerful words in medicine, and likely words that these people with chronic pain have never heard. Most importantly, they satisfy the ultimate goal of TNE:
Reduce the perception of threat
That, my friends, is what all physical therapy interventions do. Exercise, manual therapy, and education all reduce threat perception. These simple words can often jump start the process.
Fear and catastrophization are often the big components that we have to battle with the above patients. When these beliefs regarding pain are present, a cycle of avoidance and disuse occurs. These factors can continually perpetuate the pain cycle.
When experiencing pain, we can go one of two routes.
We can see how understanding pain can have profound impacts regarding recovery, yet the converse can lead to a debilitating cycle. Our goal is to steer people towards confronting their experience as quickly as possible. Knowledge can be powerful at reducing chronic pain.
Realize that there are many other factors that go into which path one will travel. These factors may include pain beliefs, sleep, behaviors, family, social circle, job, etc. These examples are a few of many variables that make pain as complex as it is.
The best that can be done is to manage the threats you are able to influence and educate the patient on understanding other possible factors.
Now some of you psychology fans might be thinking that this strategy may be stepping into areas outside of our scope. But think of how we treat impairments that may be impacting one’s movement:
Stiff joints – manual therapy
Altered muscle recruitment – motor control
Muscle stiffness –manual therapy
What if the impairment impacting one’s movement is one’s thoughts and beliefs? What intervention would you utilize to address this area?
Clockwise ultrasound of course.
The logical choice of course, would be educating the patient that these thoughts and beliefs do not relate to the pain experience. Successful education may affect the impairment shackling that person.
Why is it that when patients come to us in pain we teach them anatomy? This was a question Adriaan posed to the class that summed up my frustration with much of traditional orthopedics in a way I never could.
There are a few studies (here and here) that have demonstrated that educating patients on anatomy and biomechanics has limited efficacy and may increase fear. Moreover, using degenerative terms are associated with poorer prognosis (here).
The problem with this strategy is that it does not adequately address what the patient is seeing you for–pain. Fortunately, the evidence for TNE is becoming quite compelling (check it).
It’s All in the Delivery
So TNE sounds all well and good, but the question must be posited: how? There are several ways to skin this cat (as long as the cat gets skinned):
Research demonstrates only performed by PTs currently.
Sessions can last from 30 minutes to 4 hours, but Adriaan suggested 10-minute increments.
1on1 is best, but groups of 8-10 people are also good.
Use props – pictures, drawings, metaphors, etc.
The research also demonstrates that certain content must be covered:
No reference to anatomical or patho-anatomical models.
No discussion of emotional or behavioral aspects to pain.
Nociception and nociceptive pathways.
Plasticity of the nervous system.
One phenomenal way to gauge if patients understand your education is by having them fill out the Pain Neurophysiology Questionnaire (PNQ). This tool covers a large portion of TNE, and can give you talking points on where your education ought to be targeted.
I have been having patients fill this out for a few weeks now, and it is amazing how many people have pain misconceptions even after I perform TNE. Most of the learning that was occurring was superficial. This tool gives you reason to reinforce your education, as well as a way to have evidence of learning.
Now I have been talking a lot about education, and the common misconception is that all you do is talk to your patients. This thought is far from true. Most of the study designs in Adriaan’s systematic review had other interventions along with education. So it is only one piece of the puzzle. You do not have to completely change how you treat patients, you must only change the framework at which you educate and think.
Pain Neuroscience…Learn It!!
If you are going to explain pain to patients, you have to know more about it then they do. To enhance our knowledge base, we can discuss the PNQ in detail. So fill it out before reading on.
Go ahead, I’ll wait.
Did you fill it out yet?
Okay, here we go:
Pain receptors convey the pain message to your brain: FALSE
Why – Tissues only send danger messages. Compare suffering an ankle sprain on a sidewalk versus a busy street. The latter would not necessarily hurt.
Fun fact – There are no unmyelinated nerves in the body. Every axon wears a coat; it just depends on what degree
Pain only occurs when you are injured: FALSE
Why – Injury and pain are not synonymous. Think about when you get a bruise and are not aware of it.
Fun fact – Tissues heal in 3-6 months. This includes your bulging discs.
The timing and intensity of pain matches the timing and number of signals in danger messages: FALSE
Why – This statement predominately deals with descending modulation and interneurons. In acute pains that end quickly, danger messages make their way up to the spinal cord and then the brain, but the brain sends endogenous opioids down the system to turn the dial down on danger messages.
There are many other fibers that that send messages to the brain, one example being A-betas. These sensors carry information regarding light touch for example. If you occasionally feel that you are wearing pants (unless you are not), you can thank these fibers.
However, you don’t have to constantly be reminded that you are wearing pants, so an interneuron in the spinal cord will prevent this information from reaching the brain. The interneuron is like a club bouncer; only the VIPs pass.
However, if danger messages (via A-delta and C-fibers) continue firing to the spinal cord, the interneuron could potentially die from amino acid overload. When this change occurs, the club called your spinal cord has no bouncer, thus all information from the periphery will make it to the brain. This input barrage can significantly impact your body’s ability to modulate danger messages, and eventually pain.
Fortunately, interneuronal death takes months to years in most cases except when someone gets struck by lightning, electrically shocked, or in whiplash. But the message is clear; we must do what we can to modulate nociception and pain so this change does not occur.
The best way to treat chronic pain is to prevent it.
Nerves have to connect to a body part in order for that part to be in pain: FALSE
Why – Phantom limb pain, duh! The somatosensory homunculus is what allows for this phenomenon to occur.
When areas are used less, such as in pain states, the area of that body part becomes less clear. These changes can occur as fast as 30 minutes. The research shows the more “smudging” of these areas you have, the more pain you have.
So in phantom limb pain, the body part is gone, but the brain representation of that area remains.
In chronic pain, the central nervous system becomes more sensitive to danger messages from tissues: TRUE
Why – Interneuron death plays a role, but also descending influences from the brain contribute. Because more danger messages are occurring, the brain is less likely to utilize endogenous opioids to calm the system down.
From a survival standpoint this makes sense. In chronic pain, the future becomes less certain, and your top priority is to stay alive. If I can make you more sensitive to your environment, I can better protect you.
The body tells the brain when it is in pain: FALSE
Why – The brain is what produces pain. The body can only produce danger. The brain activates many areas in the pain experience, making pain multi-sensory. And the more this pain map is run, the more efficient your brain becomes at producing it.
Fun fact: The amygdala’s role in pain could be why females have more chronic pain than males.
The brain can send danger messages down your spinal cord that can increase the danger messages going up the spinal cord: TRUE
Why – If there are enough danger signals reaching the brain, the brain will want to know more; thus impacting the periphery.
Nerves can adapt by increasing their resting level of excitement: TRUE
Why – Action potential are key. Every nerve has a resting amount of activity, and a certain amount of stimulus is necessary before this action potential occurs.
When someone is extra sensitive, the nerves increase their resting excitement level so action potentials more readily occur. Adding more ion channels to less myelinated areas can further compound this sensitivity.
Fun fact – Ion channels change every 48 hours, and therapy can positively influence the change.
Chronic pain means an injury hasn’t healed properly: FALSE
Why – Read, like, everything I have ever written ever. Pain and injury are not the same thing. Tissues heal, tissues heal, tissues heal.
Receptors on nerves work by opening ion channels in the wall of the nerve: TRUE
Why – See above.
The brain decides when you will experience pain: TRUE
Why – Pain is a brain construct. Tissues can only send danger messages.
Fun fact – Laughing at a joke requires 5 different areas to be active in the brain.
Worse injuries result in worse pain: FALSE
Why – See video below
When you are injured, the environment that you are in will not have an effect on the amount of pain that you experience: FALSE
Why – Injuries and pain occur in an environment, not a vacuum. An ankle sprain may hurt on a sidewalk, but likely won’t if a bus is about the hit you.
Fun facts – Injuries in high stress environments are 7-8 times more likely to produce chronic pain. Also, kids who play contact sports early in life have less chance of developing chronic pain.
It is possible to have pain and not know about it: FALSE
Why – Pain is a conscious decision by the brain. No brain, no pain.
Nerves can adapt by making more ion channels: TRUE
Why – I already answered it duuuuude.
Second order messenger nerves post-synaptic membrane potential is dependent on descending modulation: TRUE
What did I just say? – I don’t know.
Why – The brain has the abilty to inhibit information coming up from the periphery via endogenous mechanisms. This is how placebo works.
Nerves adapt by making ion channels stay open longer: TRUE
Why – Because I said so…directly above. The brain will also make g protein ion channels, which can stay open for several minutes. This type allows for more danger messages to fire.
When you are injured, chemicals in your tissue can make nerves more sensitive: TRUE
Why – Much was previously mentioned, but the stress response plays a huge role here. When you go into a more sympathetic state, adrenaline, cytokines, and cortisol pump throughout the body. This change increases sensitivity of nerves throughout the body systems, and those in chronic pain are more geared toward this state.
Put it all together, and what do you got???
So with all the above information, we can see there are many misconceptions regarding pain. So it becomes very important to define what pain is. Here is a great definition:
“Pain is a multiple system output activated by an individual’s specific pain neural signature. The neural signature is activated whenever the brain concludes that body tissues are in danger and action is required.”
So Let’s Do Something about It
While we do need to know all the nitty-gritty regarding pain physiology, your patients and clients will not know what the heck you are talking about. Thus, you have to teach this information in a patient-friendly manner. Here were some of my favorite ways Adriaan used for TNE.
You can also mention to patients in chronic pain that one in three people keep their nerves elevated past normal healing times.
With this example, there are usually three questions that arise:
How do you know this?
Why did my nerves stay/become so sensitive?
What can be done to calm them down?
Number one can be answered by the following points:
You told me – it takes less activity for pain to arise.
Your tests told me – physical exam and neurodynamic tests.
Your doctor told – any anti-depressants or drugs like Cymbalta or Lyrica can calm the nervous system down.
We can answer number two by having them think about the many factors that could enhance sensitivity. These factors could be failed treatments, hearing different explanations, pain chronicity, life worries; basically anything that could make you feel threatened.
Number three is easily answered by explaining the powers of education, exercise, and medication.
The Old Speeding Bus Trick
Say you sprain your ankle. Would it hurt? How about if a bus was about to run you over? This tactic demonstrates that the brain makes a conscious decision as to whether or not pain should be experienced; and the greater threat always wins.
I Hate Having Neighbors
Here is a great way to explain spreading pain to patients.
Say your alarm goes off and you begin to feel pain. If your alarm stays on long enough, the noise may wake up your neighbors. If the neighbors stay awake because your alarm keeps going, eventually they will get agitated. It wouldn’t be surprising to see neighbors even farther away waking up if the alarm stays on too long.
You can also tie in the immune system in to this example. Immune molecules are like little police men that check out everyone and make sure the situation is okay. Nearby neighborhoods might also be checked out just to be safe.
The police watch the area until the problem is taken care of. But as is customary, a few months later the police may check-in to make sure everything is okay. This analogy can explain why pains you once had can reoccur.
The Road Often Traveled By
This analogy is a great way to show how chronic pain allows for neural pathways to turn on more efficiently.
Think of a neural pathway that would lead to a pain experience as a dirt road. If you get a lot of traffic along that pathway, eventually the road is going to have to get bigger to accommodate. So perhaps the road is widened. Maybe the next step is the road getting paved, then making the roads 2-laned, etc.
The more that pain pathways run, the more fluidly they do so. The pain experience is created faster and faster with the more traffic encountered.
The Top 5 Reasons Why a Bulging Disc Ain’t a Big Deal
You are inevitably going to run into someone who thinks having a bulging disc is a death sentence. Here are the 5 facts (in order) that you should mention to them:
6 weeks after a scan is performed bulging discs become smaller.
You can get completely different results depending on the time of day the MRI was taken; early am is more likely to show disc bulges.
Position MRI was taken in affects results.
Levels that swell don’t move much; thus laying still or moving can impact results.
40% of asymptomatic individuals have bulging discs.
Two Lions Walk into a Bar…
This analogy is a great way to explain the stress response. Imagine you are watching television minding your business when a big African lion walks in the room. What happens to your body systems?
Adrenaline pumps through the bloodstream, increasing heart rate, breathing, alertness, etc.
Big strong muscles turn on; smaller muscles turn off.
Raise voice and speak short and sharp.
Shallow and fast breathing.
Reproductive systems stop (unless you dig lions)
Many other things.
When the lion leaves the room, the body returns to its previous resting state. Chronic pain states is akin to having this lion following you at all times. This state, which can be perpetuated by many factors, can keep the above changes going relentlessly. Our goal with therapy, is to make that lion less threatening.
While we have been exposed to great science and metaphor, the practical component was what did it for me. Adriaan had so many wonderful suggestions for implementation that I had to list some of my favorites:
Train the entire staff on TNE; including front office.
Designate particular days as TNE days.
Can teach in 10 minute increments.
Carefully use the word pain. Asking patients pain rating repeatedly may increase pain ratings.
Have a strict cancel/no show policy: Adriaan likes one cancel; >10 minutes late leads to a reschedule.
No more than 5 exercises for HEP.
Aerobic exercise is huge for chronic pain. Perform at >50% VO2 max and >10 minutes.
A big one for me regards coping skills. Before a patients calls in on a bad day to see a therapist, 5 strategies should be performed first:
Problem solve – find a cause/relationship.
Perform your exercises.
Get away – walk for a little bit, then relax and take a cleansing breath.
Do not cancel all activities. Do as much as you can.
Quotes from Adriaan
“Light a candle, watch Oprah.”
“The holy grail to chronic pain is prevention.”
Take that patient. Own that patient. Fight for that patient.”
“Your challenge is to be so good a these [chronic pain] patients that the other stuff will become mundane.”
“If you are a PT and have not had back pain you are dead to me.”
“Aerobic exercise is gold standard for chronic pain.”
“Parenting sets up pain later on.”
“The biggest boost for the immune system is social interaction.”
“Low back pain is the common cold of the musculoskeletal system.”
“Your job is to make your patient so smart that pain decreases.”
“30% of pain is insidious onset”
“You are not treating evidence, you are treating a patient.”
“The best clinical question you can ask is ‘what do you think is going on with your x.’”
“Make patients responsible for their own care.”
“The bigger threat wins.”
“The biggest predictor of chronic pain is acute pain.”
“pain spreading is an expansion of receptor fields.”
“When pain is involved motor control becomes 2nd.”
“Pain is a unique human experience.”
“If you live your pain, you become very good at living your pain.”
“Don’t forget the human being.”
“You are a walking placebo pill.”
“Lyme disease is the new fibromyalgia.”
“A brain that doesn’t know is the most dangerous thing on the planet. Make the unknowns known.”
“Pain is what I think.”
“You own your pain.”
“If you teach about pain and they feel worse, you got them.”
“Chronic pain patients are not weak, they are deconditioned.”