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.”
I have come pretty far in my journey since initially being treated at the Hruska Clinic (see day one, two, and three).
I have developed a beautiful squat, am noticing less back issues when I lift, and just generally feel mo’ betta. I also have zero fatigue when reading or on a computer screen.
That said, I was still getting some right neck tension and felt that my reading comprehension was not as good as it was.
I was accommodating to both my orthotics, so I thought my next trip to Lincoln would be a good time to follow-up.
If Youz Ain’t Assessin’ You Guessin’
Came through the door after a long flight and minimal sleep, and surprised even myself.
Without any orthotics, I was neutral at my pelvis and thorax, but still had some left cervical axial rotation and right OA sidebending restrictions.
I was also lacking the capacity to perform mandibular lateral trusion without kicking in my SCMs. The reason why I don’t have access to my pterygoids for this movement?
Those DAMN wisdom teeth.
My wisdom teeth essentially alter pterygoid position and reduce my mandible’s capacity to move. When I protrude, I have to extend my OA joint and utilize a forward head posture to complete the movement.
The same thing occurs with lateral trusion. When I attempt the movement, the bony block limits my pterygoids from performing the action. SCMs, in particular the right, try to pick up the slack.
From a visual standpoint, I was sitting pretty. I didn’t really have much trouble with far vision, and when Heidi checked my close vision my eyes were working symmetrically.
The fix for me is still wisdom teeth extraction (which is happening in October of next year), but was there anything else that could be done until then?
“There’s one more thing we can try.” ~ Ron Hruska
I see Ron place a pole out in the PRI vision hallway and he has me stand and stare on the right corner of a doorway.
“How far away does that appear?”
I said it was about 6 feet away.
I did the same exact thing on the left side of the door, only this time the pole appeared a couple feet farther away.
Having that slight depth perception asymmetry was my last saving grace before teeth extraction, as this was how we were going to give me a little bit more frontal plane.
They fit me with some very lightly prescribed lenses and focus on evening out my depth perception. The way that I do this is by activating my left SCM with right cervical rotation and then moving my eyes to the left. I also do the reverse. This activity is to be done on either side of a doorway so I alternate from looking at close and far space.
Just doing this exercise a couple times a day has already quieted my right neck down quite a bit, so I am hopeful that this will carry me the next several months until surgery.
I will now be doing extra-ocular muscle day at the gym in place of back and bi’s.
In terms of reading, we tried some evened out lenses but I couldn’t really tell a difference in terms of comprehension. What actually made the largest difference for me was taking my splint out and reading. Ron said that the splint is used to create movement for me, so was probably not necessary when I read. I just have to remind myself to contact my teeth every so often when I am reading.
The Game Plan
Aside from the little activities above, I am discharged from PRI vision. I only need to come back if I get some visual changes after I get my wisdom teeth out. From here on out it’s all about getting my EOMs jacked, alternating activity, and wearing my splint less.
I really enjoyed this course because it was such a high-level affiliate and great prep for my PRC. We went into great deal regarding position, throwing mechanics, and treatment.
One of the most amazing pieces of the course was Allen’s ability to breakdown complex baseball movements into their basic biomechanical bits, And from that point show what compensatory things could occur if limitations are present. His eye for these things is unreal.
That piece of the course is a post or two on its own, so I won’t touch it here. In fact, I probably won’t touch it at all. Go to this great class and be wowed by Allen. You will be motivated to become a better clinician. I know I was.
Here are some of the big takeaways.
PRI 101 v 3.0
I’ve heard this overview three times this year now, and it is amazing that I still pick up things from it. James really outdid himself here.
The big piece this time around was space. We want space maximized.
In the vision course we discussed maximizing left peripheral visual space because the pattern reduces this quality. The pattern in general reduces our ability to move through triplanar space.
There are a few other reasons that we would be unable to shift into our left side. Overactive muscles chains may prevent this action, but we also have something very large occupying the left side.
We call this thing air.
If we are hyperinflated in particular areas (think left chest wall), how can we expect to go to the left side? Left space is already filled with air. Airflow must be transferred to the right side in order for us to maximally close down our left. Maximal left sided closure via a zone of apposition is necessary to create true left stance.
Patterns, Adductors, and Pecs (Oh My)
The right adductor magnus and left pec major, though not part of the LAIC/RBC pattern, are still very active muscles. Why is this so? These muscles prevent falling over when in right stance with left trunk rotation.
That PRI Doesn’t Work, I Got Someone Neutral and they Felt Worse
False! Here’s why.
An individual’s norm when under threat is the LAIC/RBC/RTMCC pattern. It’s autopilot; it’s what’s comfortable.
Let’s say you take that away from someone. They have greater movement freedom, but are not sure what to do with it or how to control it. This change could be perceived as a threat by the brain, and symptoms may increase as a means to prevent movement exploration into this new space.
I tell my patients when this happens it is like they just got their driver’s license and I gave them a Ferrari.
A Ferrari is a little more challenging to drive than most cars (so I hear, that blog paper hasn’t hit that level yet), so it’s going to be a bit harder to handle. Once the patient learns how to drive the Ferrari the possibilities are endless.
They must learn a new pattern (RAIC/LBC/LTMCC) in a nonthreatening manner so they obtain locus of control in this new position. Once integrity is achieved here, alternating reciprocal activity is ingrained to maximize movement variability.
Pattern Pitching Problems
Depending on what arm you throw with, you are going to have a bit more trouble with certain aspects of pitching movements. I won’t go into the bazillion reasons why this happens like Allen did (go to the course yo), but here is what each throwing phase needs.
If I’m a right-handed pitcher, the LAIC/RBC is going to limit me. Let’s break it down to each throwing phase:
Wind-up – Need to turn on right posterior glute med to delay LAIC activity.
Stride – Need to inhibit right adductor and QL to maximize stride length.
Cocking – Need to shift into Left AF IR while maintaining right trunk rotation.
Acceleration – Need to keep Left AF IR in trunk flexion.
Follow through – Need to balance into left AF IR.
If I’m a left-handed pitcher, the RBC, posterior mediastinum, and timing will be my largest limiting factors. Here is what I need at each component of throwing.
Wind-up – Need to load left AF IR and engage abs to stay back. Inability to do this is what creates that beautiful natural spin us lefties have when we throw.
Stride – Need to inhibit LAIC/RBC so one does not rotate too early into Right AF IR and right trunk rotation
Cocking – Need to control Right AF IR and left trunk rotation while reducing back extension and keeping adequate left posterior mediastinum activity.
Acceleration – Need to keep trunk closed down into flexion
Follow through – Need to balance into right AF IR.
Repetitive Rotation Superior T8 (Gasp)
This part was probably the most controversial and misunderstood piece of the course. The concept itself is not difficult to understand, but the material may seem challenging to fit into the PRI philosophy.
I’ve had several discussions with James Anderson on this topic to make the masses get the most up-to-date explanation for this pattern. Here is what we came up with [My post-conversation thoughts will be in brackets].
In the first two baseball courses, “repetitive rotation superior T4 syndrome” was used to describe a rare compensatory pattern seen in particular populations. James and Allen are now calling this pattern “repetitive rotation superior T8 syndrome.” The name changed because there are more ribs reversing the underlying LAIC/RBC pattern then the top 2-4 ribs. This change will be in all future baseball course manuals.
And now for the condition itself. There are certain instances, albeit rare, in which certain individuals may appear to have a reversed posturalpattern (RAIC/LBC). Repetitive right trunk rotation occurs via various trauma and/or functional demands, such as the deceleration thru follow-through pitching phase for a lefty or the back swing for a right handed golfer, creating a thorax that is driven to the right.
You can also see this in PRI junkies who bias the left side only and never alternate [Like a right-sided hemineglect neurologically. If right-stance activities are not appreciated, variability may lowered possibly due to disuse. One possibility for this is also losing appropriate right zone of apposition while in left AF IR, to which I will discuss in a future post].
This T8 syndrome differs from classic superior T4 because more drivers push the thorax to the right and externally rotate the right ribs. In the T4 case, the scalenes elevate the upper 2-4 ribs to meet excessive respiratory demands. In T8’s case, the left BC kicks into high gear and drives more of a PEC/bilateral AIC pattern. It may mimic a RAIC/LBC, but not be the case.
With the thorax rotating hard to the right, the pelvis and lumbar spine must orient left and into a pseudo-left AF IR translatory-type movement. Consequently, these folks stand and function quite well on their left leg compared to the right.
Seeing a “flipped” pattern is nothing to freak out about; there are still underlying LAIC/RBC patterning at play. This repetitive rotation superior T8 syndrome is an atypical compensatory strategy that requires atypical treatment.
Interventions basically flip normal PRI activities; shifting into right stance with left trunk rotation. We technically cannot call this “PRI” because the underlying human asymmetry is not addressed.
Treating in this fashion does however put the system into a “normal” asymmetrical pattern to which conventional PRI methods can be used. [That said, the name of the game has always been alternating and reciprocal activity. Everyone should be able to do traditional PRI activities on both sides without falling apart. The reason why this is not called PRI is because of the order treatment occurs in].
[The big message at the end of the day: Trust your measurements and treat accordingly].
Elbow and Wrist Drive Thorax
This portion was one of my favorite pieces of the course; namely because it’s not talked about anywhere else in PRI land.
There are 4 possible patterns on the left and right side that can occur at the humeral-radial joint; depending on the position of each.
I won’t go into details on each, but basically if you see increased mobility in one direction (supination or pronation), you likely want to inhibit that direction and facilitate the converse.
Wrist flexion, pronation, and internal rotation facilitate serratus anterior and contralateral thoracic rotation.
Wrist extension, supination, and external rotation facilitate lower trapezius and ipsilateral trunk rotation.
Reference centers in the wrist and hand can also be used to facilitate position. When attempting to facilitate left stance with right trunk rotation, use a right pisiform and left palmar arch.
So there you have it. Some of my favorite pieces from this excellent affiliate courses. It’s filled with a ton of information, and is easily the most challenging conceptually of the three affiliate courses I have taken. You won’t regret this one.
Great James Quotes
“If you see a forward head, hand them a card that says exhale please.”
“Inhaling in a state of exhalation is neurologically cool.”
“It’s not magic. It’s better than magic. It’s neurologic.”
“We’re gonna talk about trauma called throwing a baseball 95mph with your left hand.”
“That muscle firing is a total waste of sarcomere slide.”
“Your brain is a better parent of your body than I was my son.”
“Ron is looking at the brain, not the plumb line.”
“A plumb bob and grid is offensive to Ron Hruska.”
“What have you thought about the fact of never blowing up a balloon as a grown man?”
“He sucked a lot of balloons empty.”
“Hand on the heart for serratus anterior. Go ahead.”
Gruv-y Allen Sayings
“You are only as good as your patient will allow you to be.”
“I can’t stand research to a point.”
“The right QL and adductor are best friends…Just like James and I.”
“Don’t judge someone just by video.”
“You can’t make a program based on a screen.”
“If you’re not doing test-retest give them they’re copay back. You are failing them.”
“One pound dumbbells are not changing my patient’s lives.”
You’d think, but CCM is one of the hardest PRI courses to conceptualize.
It didn’t hurt that my work was hosting the Ron’s last time teaching this course, as next year we will see Cervical Revolution instead.
I took this course last February, and it’s amazing how different the two courses were. We had a room filled with PRI vets, and the Ronimal went into so much more depth this time around.
It was such a great course that I would love to share with you some of the clarified concepts. If you want a course overview, take a look here.
The right TMCC pattern consists of the following muscles with the following actions:
Cranial retruders/mandibular protruders
Right anterior temporalis
Right medial pterygoid
Left rectus capitis posteror major
Left obliquus capitis
OA flexors that maintain appropriate cervical lordosis
Right rectus capitis anterior
Right longus capitis
Right longus colli
If this chain stays tonically active, then there is better accessory muscle respiratory capacity present. These muscles provide the fixed point needed for an apical breathing pattern.
We want the muscles on the other side, the left TMCC, to be active. Their activity will allow alternating reciprocal cranial function to be possible.
We also call this gait.
Keep Ya Sphenoid Flexed
One cranial goal we have is to achieve sphenobasilar flexion, but what does this mean?
In the RTMCC pattern, the sphenoid is in an extended position. When the sphenoid is extended, the foramen magnum becomes larger and the spinal cord descends. This positioning explains all the chiari malformation jokes that we like at PRI-land.
This position would also create a forward head posture to create a compensatory airway. Consequently, occlusion may be altered.
The goal is to flex the sphenoid, which closes the foramen magnum and produces appropriate OA extension. This position keeps the brainstem happy.
Lordosis is Important
When the SCMs are overactive, especially on the left, a reversed cervical lordosis can occur.
If I see someone who cannot flex his or her neck, I’m not thinking of stretching them into flexion. I’m thinking about restoring cervical lordosis. If no cervical curve is present, then the neck is already at end-range. Stretching farther in this position could create potential pathology.
Lordotic position is achieved by the deep neck flexors listed above and maintained by a twisted levator scapula position under a foundation set by an active lower trap.
I learned to appreciate the SCM much more at this course.
In the RTMCC pattern, my OA joint is sidebent to the left. This position occurs due to the left SCM, rectus capitis lateralis, and levator scapula.
When an active left SCM is present, we usually see a corresponding frontal plane positional tug occur at the thorax and pelvis. Left SCM often works with the right quadratus lumborum and right adductor to push the sphenoid, sternum, and sacrum into a right lateralized state.
Pterygoids = Money
When lateral trusion in protrusion is assessed, we are not really assessing jaw mobility but pterygoid function.
The left lateral pterygoid moves the mandible anterior and to the right no doubt, but it also moves the cranium posterior and to the left. We call this left acetabulofemoral internal rotation aka shifting into your left cranium.
This Really Bites
We discussed a lot about bites this weekend. One bite that would most certainly need dental integration is an anterior open bite. This bite is when the front teeth are unable to contact due to a very high palette.
This bite type would be the equivalent of rib flares on a PEC individual. When one has an open bite, the mandible retrudes far enough to increase pressure onto the mandibular condyles.
The TMJ essentially begins to act like a molar.
We also got to see an individual with a cross bite, in which the part of the teeth go so far inward that teeth contact occurs at an angle.
This positioning is very similar to the feet in a left AIC pattern. The right foot is in a supinated position, but the first ray will oftentimes create first ray plantarflexion to touch the ground. A cross bite is a similar phenomenon.
Other Fun Clinical Tips
The louder and earlier the click upon TMJ opening the healthier the joint is.
Front teeth contact keep temporal bones alive.
Back teeth keep head from going forward.
(in)Famous Ron Quotes
“I’m not interested in your 45 mm of opening.”
“I’ve learned one thing in life. Jaw surgery does not work.”
“I call it the quadratus eboli.”
“We’re going to talk about sciatica of the head.”
“You know, my mother is not so bad after all.”
“I want you to take this course because this is life.”
“I’ll say feeling cerebrospinal fluid is a bunch of you know what.”
“If you’re a mammal you suck. You suck as a mammal.”
“If you don’t suck you don’t have a neck.”
“Are you a mammal? No Zac you’re weird.”
“The IC lateral pterygoid. Oh sorry wrong course.”
“You didn’t know getting your IC adductor would help you taste Pepsi better?”
“Guess I’ll go to PT school. Maybe I’ll learn something there. NOPE!”
“The best thing you can do is invest your retirement dollars on CPAP machines and ambien.”
“The system knows everything.”
“This patellar, excuse me, temporalis region.”
“Buy some Bose headphones and listen to Lady Gaga. Wow! That worked.”
“I just walked you through evidence that has been there for years and no one can handle it. Oops.”
“Surely. Don’t call me Shirley…Sahrmann.”
“I’m not here to recapture someone’s disc…Oh but I am.”
“The biggest shim that anyone does is a heel lift and it makes me want to puke.”
“If you have one foot that pronates and one that supinates, you’ll need a podentist.”
“The number one concussion is the Iphone.”
“Salt, pepper, and left lateral pterygoid.”
“I want his pube to like his malleolus. Oh I didn’t mean that.”
Several different thoughts have crept into to my mind sparked by what I have read and conversations I have had. I would like to share these insights with you.
I remember when I was visiting Bill Hartman Dad a few months ago and we were talking about a specific treatment that is quite controversial in therapy today. He said something that really resonated with me:
“Thus, pain can be viewed as a single perceptual component of the stress response whose prime adaptive purpose is to powerfully motivate the organism to alter behavior in order to aid recovery and survive.”
Notice what I bolded there. Pain is a single component of the stress response. Not the stress response. Not a necessary component of the stress response. Just one possibility.
Why do we place so much importance on pain?
Many proponents of modern pain science (myself included) often use this statement against individuals who are over-biomedically inclined:
“Nociception is neither necessary nor sufficient for a pain experience.”
Agreed, pain is not always the occurring output when nociception is present. That said, pain is only one of several outputs that may occur when a tissue is injured. Just because pain is absent does not mean other outputs are also absent.
Many different outputs can occur when an individual is under threat.
Let me propose a new quote to those who focus solely on pain.
“Pain is neither a necessary nor sufficient output of the stress response.”
Why should we limit ourselves to only treating pain? Why should we limit ourselves to only treating outputs? (Spoiler alert, we can’t treat outputs, change them) I have a better idea.
Today, I start treating a human system under threat.
The Threat Matrix
Dad showed me this great editorial here in which Eric Visser expands upon Melzack’s original pain neuromatrix.
Visser calls this idea the threat matrix. To simplify the idea, threatening inputs from the body and the environment enter the system, are scrutinized by the brain, and then the desired output to combat the threat occurs.
Input –> processing –> output
This framework explains how any output, desirable or undesirable, can occur from a stressful input.
Let’s apply this to an example that we have all been through; a breakup with a significant other.
Your significant other decides to leave you, how do you feel?
The answer depends on the individual. Some folks may feel depressed. Some may feel anger.
Some may even experience pain.
These feeling are all outputs that occur as a result from an input (i.e. the breakup) that disrupts homeostatic balance of the human system. The outputs that occur are the ones that the brain determines best aid the individual in recovery and survival.
Let’s now take this thought to the therapy realm. I sustain tissue damage and nociceptive information travels to the brain to be scrutinized. What output(s) could occur? Let’s think of a few possibilities.
Endocrine alterations in gut/reproductive function
Increased/decreased immune activity
Yada yada yada
All of these could occur, some of these could occur, or none of these could occur. The response to the offending input is going to depend on the individual’s brain scrutinizing the situation.
One could argue that a nociceptive event could lead to someone developing anxiety and poor immune function without ever experiencing pain if that is what the system feels best aids in survival.
Nonspecific Effects my Arse
There are many treatments out there that people deem worthless because research demonstrates minimal effects on pain compared to placebo. If someone gets better with this intervention, we deem that nonspecific effects led to the change in pain.
I call bullpoop…sort of.
Nonspecific effects could be a contributing factor to someone benefitting from a particular treatment, but the problem with most pain research is that often pain level is the only thing that is measured.
If pain is only one possible output of a system under threat, how do we know that a treatment didn’t affect a different output?
Answer: We don’t because it wasn’t measured!
Let’s take a controversial treatment for example: dry needling.
Some say it works wonders for pain, some are vehemently opposed, and research is mostly mixed. What do we do?
Perhaps both camps are wrong. Why? Pain is the only output being discussed.
What if this whole time, dry needling worked because it altered inputs coming in from the immune, autonomic, or [what the hell evahhhh] system, which led to changed output from this system primarily with pain output altered secondarily? And here is the kicker; the intervention only works if these systems respond as well as our pain system under a particular threat.
Well we don’t know that because we didn’t look at it. But looking at multiple systems when an intervention is implemented may give us more explanatory power as to why certain treatments help certain individuals. With this information, treatment could be streamlined and implemented.
Making pain our only concern to treat severely limit our capacity to help individuals. If we think of treating the stress response itself, we open up a huge realm of issues our interventions may affect.
If you take a look at the book “Spark” and the corresponding research, we see how exercise can alter many different outputs.
Why can’t rehab folks be a piece of this puzzle? It does not seem unreasonable to me that we could get referrals for anxiety, depression, or whatever output the stress response creates.
Strategically implemented exercise can help alter the stress response. That possibility makes me so hopeful for our professions.
How can one best assess a system under threat?
If clinicians are to assess if an individual is undergoing a chronic stress response, we need to find a reproducible methodology that gives us this information. We must look at the human system from the input/output standpoint.
There are several outputs that can be measured to assess an individual’s homeostatic state:
Other specific medical tests
These are all great tests that can assess the amount of system stress an individual is undertaking. That said, I feel there is an even simpler method of assessing the stress response:
Our physical examination
Assessing the stress response begins with the subjective examination. This piece of the clinician-patient interaction helps us assess potential offending inputs as well as individual processing.
If we come across red or yellow flags, we can easily refer out to providers who can deal with that piece of the stress response. Here is where a psychologist, surgeon, oncologist, other medical professional can come into play. These individuals can alter the offending inputs or help influence processing that therapists and the like may not be able to touch.
Let’s say we get through our subjective and we screen out that the above professionals do not need to be a part of this person’s care. Let us now proceed to our objective examination.
Assessing movement may be the simplest way to assess an individual’s stress status.
If we are to provide the “ideal” physical examination, we need to perform tests and measures that best differentiate a stressed from nonstressed individual.
To undertake this task, we need to have a few assumptions about what a nonstressed individual looks like. Let’s call this individual the “adaptable human.”
The adaptable human will have desirable multi-system variability. That is, human systems can perform as needed under certain situations without being “stuck” in a particular range. For example, blood pressure should stay lower when at rest and rise when performing physical activity. When blood pressure remains high at rest and with physical activity, that individual possesses system rigidity.
The adaptable human will have desirable multi-system capacity. That is, human systems can tolerate prolonged stressors without faltering. For example, a human can perform longer durations of physical activity with blood pressure remaining in levels that would not threaten one’s life.
The adaptable human will have desirable multi-system power. That is, human systems can tolerate intense stressors without faltering. For example, blood pressure can reach a desired level to allow for a particular physical activity to occur.
Our examinations ought to assess these three qualities: variability, capacity, and power.
Of the three, variability is most fundamental because almost every healthy human system functions in the manner. The movement system is no exception to this rule.
Movement variability, the ability to move in three planes, is the simplest reflection of this concept. A nonstressed system will possess movement variability. A stressed system shall become rigid and lose triplanar mobility.
Think to the last time you were stressed. Did your muscles tense or relax? As muscles tone increases, range of motion decreases. Assessing movement variability is an easy way to assess the general tone an individual has, and I speak more of why this notion is favorable here.
To assess variability, our examination must:
Look at the entire individual’s body
Cannot have bias toward one output (e.g. pain)
Must be reproducible and predictable
First, let’s look at popular rehab systems that I feel would not work in this instance and why.
Maitland: Biased toward altering one output (pain); segmental in nature.
McKenzie: Biased toward altering one output (pain); segmental in nature.
SFMA: Not necessarily biased toward one output, but does not look at entirety of human movement. Only two movement planes are assessed. Cannot see if an individual has variability in the frontal plane.
DNS: Wait? Do they even assess?
I shall let my bias now creep in as I suggest the current best model we have for movement variability is PRI.
There are several reasons why I think PRI is currently the best model to assess threat:
It is not biased toward altering one output, as movement rigidity can occur along with several other outputs besides pain.
The entire human movement system is assessed in three planes.
The protective patterns one undergoes in threat are predictable and similar for all individuals.
When one deviates from these patterns, likely pathology had to be created in order to do so.
If an individual can produce nonpathological triplanar movement throughout his or her body, then movement variability is present. A movement system under threat will not have this capacity. A threatened movement system will become rigid.
Establishing movement variability is our primary way to reduce threat-response outputs.
If undesirable outputs remain once movement variability is established, then we know other interventions must be given to address these areas.
If pain is still present, then previously mentioned assessment systems hold value, as does graded exposure.
That was the first interview question Ron Hruska asked me; something I will never forget.
I went to Lincoln, NE for almost a week to take a course, get treated, and observe PRI in it’s purest form.
I wanted to see Ron out of curiosity and because I cannot achieve neutrality on my own. I have done most every exercise that could be thought of and been “worked on” by my fellow comrades and a couple PRI instructors in courses; nothing could budge.
I knew I needed some type of orthotic to get somewhere; the question was which one?
I do not have any pain really. My only complaints are a tight neck and I can’t seem to deadlift without feeling most of the effort in my back.
I don’t see this deadlifting problem as a form issue necessarily. Interning with Bill Hartman at IFAST cleaned that up, and for a long time I could feel glutes and hamstrings all day when I deadlift.
But not now.
Other “issues” I have
Left TMJ clicks; nonpainful.
Clench jaw at night.
Eye strain after reading on a computer too long (duh).
By PRI standards, I am a classic PEC. I have no pathology anywhere, but I am limited in almost every motion. I knew this and so did Ron.
First Ron had me walk and was pointing out some things to my student-to-be Trevor, and then got me up on the table to check my hips.
“Here’s your problem.”
My hip external rotation was about 70 degrees on the left, 40 on the right. He then checked my hip abduction, which was a solid 30 degrees bilaterally. The next test followed in a logical progression…
He gloved up and checked my bite.
He noted I had a type I occlusion bilaterally and noticed my chipped front tooth. He wanted to show me which tooth was grinding on that, so he asked me to move my jaw forward.
I couldn’t do it.
He gave me a mirror to help see what I was trying to do.
I couldn’t do it.
He put a towel over my eyes and dimmed the room.
I easily contact my front teeth, gain 30 degrees of hip abduction on both sides, had equal hip external rotation, and for the first time ever had a negative thomas test.
We figured out what I needed.
The Needed Orthotics
Ron concluded that I was a tongue thruster, had a very narrow/crowded mouth, and my visual system was patterned enough to drive my nervous system into extension. He also explained, which blew my mind, that a reason I always put my hands in my pockets is to provide a reference center for my very active hip flexors.
My right hand is my TFL, my left hand is my psoas.
The next process was to contact his dentist to fit me for a Gelb splint and set me up with a day at PRI vision.
Before chatting with the dentist, he checked my mouth one more time just to make sure he had all the information he wanted to say. It was this second look that Ron noticed that I still have my wisdom teeth.
Pavel Kolar and crew actually contributed to quite a few chapters in this edition, and this one here was overall very well written. Believe it or not, it even had quite a few citations!
Why they don’t cite many references in their classes is beyond me, but that’s another soapbox for another day. Onward to a rock-solid chapter.
En utero, the diaphragm’s origin begins in the cervical region, which could possibly have been an extension of the rectus abdominis muscle. As development progresses, the diaphragm caudally descends and tilts forward. When the child is between 4-6 months old, the diaphragm reaches its final position.
Throughout this period, the diaphragm initially is used for respiratory function only. As we progress through the neonatal period (28 days), we see the diaphragm progress postural and sphincter function.
The diaphragm is integral for developing requisite stability to move. Achieving movement involves co-activation of the diaphragm, abdominal, back, and pelvic muscles. This connectivity assimilates breathing, posture, and movement . If this system develops properly, we see the highest potential for motor control.
The largest developmental changes in this system occur at 3 months. Here we see the cervical and thoracic spine straighten and costal breathing initiate. 4.5 months shows extremity function differentiation, indicating a stable axial skeleton to which movement may occur.
Further progression occurs at 6 months. Here costal breathing is fully established. We also have increased diaphragm and lumbar spine stability. This part is necessary for support to occur in the quadruped position, as the proximal attachment of the psoas has a firm place to pull the baby up onto palms and thighs.
In an Ideal World
Per development, an ideal breathing pattern ought to involve the diaphragm descending in the caudal direction, with elastic recoil promoting ascension upon exhalation. As a result, the organs shift caudally as well, and the abdominal wall expands in all directions.
From a muscular perspective, we see an alternating dance of muscle activity. Inspiration requires concentric diaphragm and pelvic floor activity, which compresses the abdominal cylinder to establish intra-abdominal pressure. Ab wall expansion occurs via eccentric activity of the abdominal muscles, quadratus lumborum, spinal extensors, and hip external rotators. When we exhale, the reverse occurs: diaphragm and pelvic floor eccentrically return to their starting position and the ab wall concentrically tightens up.
Regarding the ribs, we can break them up into segments that do or do not attach to the sternum. The top 7 ribs usually attach to the sternum anteriorly, thus are influenced by sternal movement.
Physiologically normal breathing involves the sternum moving anteroposterior via sternoclavicular joint rotation. It is this movement that contributes to the pump-handle activity of the upper ribs.
The lower ribs laterally expand and open during inhalation, creating a bucket-handle movement. This motion occurs because the thoracic cavity expands anterolaterally by diaphragm and intercostal muscle activity.
But Life Isn’t All Love and Happiness
Breathing sometimes can occur pathologically. One example is paradoxical breathing. Here we see the diaphragm’s central tendon become fixed, leading the diaphragm to be eccentric upon inhalation and concentric upon exhalation. As a result, the lower ribs cranially elevate and intercostal spaces narrow. Accessory muscles begin assisting the breath, creating upper rib elevation.
Because the diaphragm does not assist postural stabilization as well, the paravertebral muscles kick into overdrive to keep us upright.
The sternum begins moving cranio-caudally, the acromioclavicular joint moves instead of the sternoclavicular joint. This change is one reason why we see shoulders elevate with accessory breathing. Hence, we can see why thoracic position is important for creating an ideal environment to breathe in.
These changes can correlate to pain states. In people with chronic low back pain, Pavel Kolar found increased flattening of the diaphragm’s lumbar portion. Another study demonstrated that decreased diaphragm activity during trunk stabilization posed a greater risk for developing low back pain.
The diaphragm can play a large influence on the viscera not only from an intra-abdominal pressure perspective but with digestion as well.
The diaphragm influences eating via the vagus nerve. In order for a bolus to reach the stomach, the diaphragm’s crural portion must relax. The reverse occurs when intragastric pressure must be attained, such as when the esophagus closes off from the stomach contents. So we can see that if diaphragm activity is not up to par, there is an increased risk of gastro-esophageal refux disease occurring.
Hyperventilation disorders have been through the ringer, and to this day are hardly diagnosed. Some of the biggest classifications in my eyes arrived in 1908-09 from phsyiologists Haldane, Poulton, and Vernon. These fellows classified symptoms of overbreathing to include:
This symptom cluster occurred with respiratory alkalosis.
In 1977, Lum, Innocenti, and Cluff developed assessment and treatment programs for breathing disorders in the UK, which spearheaded breathing disorder literature.
Despite these scientific advancements, many physicians do not diagnose hyperventilation as a legitimate problem. Some of these patients even go so far as to being accused as malingering. Hearing this problem is quite unsettling, as I am seeing more and more people who overbreathe; and possibility correlating, more and more people with chronic pain. A future post is in order to show how I think the two are connected.
Breathing Pattern Disorders (BPD) and Symptoms
So many symptoms could occur with BPDs. The most extreme of these symptoms is hyperventilation syndrome, defined by the following:
Breathing in excess of metabolic requirements.
Reducing CO2 concentrations in the blood below normal levels.
Altered blood pH towards alkalinity.
Other definitions that ought to be known with these disorders include:
Hypoventilation: Increased CO2 levels due to shallow breathing.
Hypocapnia: CO2 deficiency in the blood due to hyperventilation; leading to respiratory alkalosis.
Hypoxia: Reduced oxygen supply to tissues.
Just How often Should We See This?
Probably more than you think. Hyperventilation Syndrome (HVS) is estimated to occur in about 6-10% of adults.
Of that group, women are 7 times more likely to exhibit these symptoms than men.
Many different changes occur when breathing is dysfunctional. Most notably, increased accessory muscle use and corresponding decreased tidal volume occur.
When accessory muscles are overactive, the head and shoulders are pulled forward. We also see an increase in lordosis and anterior pelvic tilt. To summate, an anterior weight shift.
Other possibilities that may occur include:
Pelvic floor weakness
Fascial restriction in diaphragm’s central tendon.
Elevated upper ribs.
Affected thoracic spine mobility and altered symptathetic outflow.
Accessory muscle hypertonia.
Cervical and lumbar spine become progressively rigid.
Function is affected in muscles that attach to the diaphragm; including the quadratus lumborum, psoas, and transversus abdominis (cough PRI cough).
With these changes, we may see a shift in body homeostasis to heterostasis if the body exhausts in attempts to adapt. It is these folks that we ought to treat.
A Clinical Case
A fellow coworker/PRI junkie of mine called me over to check out one of his patients.
This gal was complaining of neck pain, headaches, dizziness, nausea, and tingling. She had no vestibular issues at the time. She would flare up with any manual techniques to the neck or traditional headache-based therapies.
Upon observation, she presented with the above general anterior weight-shifted/extended posturing. PRI testing supported this observation.
She was given breathing exercises utilizing a balloon and straw. However, she could not breathe without extending her back. So we decided manual intervention was indicated.
Basically all we did was guide her ribs down and in to assist with exhalation; keeping the ribs down while she inhaled. The interesting thing during this intervention was that she was taking very little air in, but the amount she was exhaling was a ton. Even she was surprised by this finding.
After performing this intervention for about 5 minutes, she got up and had no neck pain. The nausea, tingling, and dizziness were also gone.
This example shows me what power breathing can have in either a positive in negative direction. This girl seemed to be in more of a hyperventilated state. By altering her breathing pattern we were able to influence this status.
Normally this drastic case is not often seen, but I feel that impaired breathing is becoming and will continue to be more prevalent.