Pain science: Part 2: How Does it Happen?

Pain Science Part 2: How does it happen?

This is finally a continuation of the previous post entitled Pain Science Part 1. As you already know, I am very excited to introduce this and hopefully be able to explain pain in relatively simple terms. The last post talked about what pain is and what pain isn’t. Now it is time to explain why we experience pain and how it all happens. Let’s start peripherally.

Input to the system includes:

Tissues

  • There is no such as a pain fiber. Tissues contain nociceptive fibers which are not pain fibers. They contain danger receptors- not pain fibers.
  • We don’t conduct pain in the periphery. We experience pain through the brain.
  • The tissues send signals to the spinal cord then up to the brain, the brain decides to call something painful or not based on its overall threat.
  • For example: If you sprain your ankle in the street you experience pain. If a bus is coming the brain will reduce the threat of the sprained ankle and make you move to get out of the way of the bus. Once you are in the clear, the pain comes back because this is the highest threat to the system.
  • Pain does NOT come from the tissue itself!
  • Another example: arthritis. Arthritis does not cause pain. How many patients have you had with, let’s say back pain, and when you have them perform exercises you can hear their knee crunching but they experience no knee pain. Pain is NOT from the periphery.

Peripheral nervous system

  • The PNS sits right below a threshold baseline. The input from the PNS either fires at a rate higher than threshold which is sent to the spinal cord or it fires just below baseline in which no response is sent further on into the system.

The injury:

  • All nerves are myelinated. When an injury occurs these myelinated axons become unmyelinated.
  • At the dorsal root of the spinal cord, ion channels are formed from DNA/mRNA and then travel down axon plasma and insert into specific areas that are unmyelinated.
  • After an injury, these ion channels form at the injury site. For example, if you develop a stress fracture/reaction in your tibia this causes a decrease in myelination-> there will then be an increase in ion channels in the area.

Ion Channels:

  • Channels open and close based upon a whole host of other influences:
    • Temperature, stress, movement, immunity, blood flow
  • They are always in a balance and if there is an increased input from one of the influences it will open the channel and send chemicals up the axon to the spinal cord.
  • For example, stress reaction= ion channels= cold temperatures= increased activity in the spinal cord. This does not = pain. Pain will be determined by the brain
  • If you are more stressed about the injury then the signal to the spinal cord will increase. If you are sick and also have this injury then there will be an even larger increase in signal to the spinal cord.
  • Ion Channels have a half-life of 48 hours. They are replaced naturally by neuroplasticity.
  • The signal is sent via chemical release from the ion channels opening. They fire in both directions. If the ion channels keep opening then chemicals are continually released to the spinal cord and can have long lasting persistent effects that have nothing to do with the current injury.
  • By educating the patients about pain, we can down regulate the system and decrease the activity of the ion channels and therefore decrease the chemicals released.

The Spinal Cord:

Path

  • The chemical released by the ion channels travel to the dorsal horn of the grey matter of the spinal cord.
  • These then are picked up by the spinal interneuron
    • The job of the interneuron is to determine what gets inhibited (stopped there) or what gets relayed up the spinal cord to the brain.
  • There are two fibers that come into the spinal cord
    • A-fibers which regulate everyday light touch activities like the feeling of your pants against your skin
    • C-fibers which are the nociceptive fibers that will alert to danger
  • The interneurons will then take the inputs and determine if the threshold is met and then either send the signal on or stop it there.
  • There is a convergence of information at this point. Not only from the left side and at the L3 level but also from the right side and everything below that level because it receives information from each segment.
    • This is why many people with chronic pain will have a bilateral presentation.

Chronic pain/sensitization

  • Persistent firing by the ion channels cause increased chemicals to be released at the dorsal root of the spinal cord.
  • This causes increased input to the interneuron, increased above thresholds signals relayed up to the brain and therefore consistent awareness down the chain at the site of the tissue.
  • This persistent input can degrade the interneuron and this also can then affect the levels around it because they are receiving even more input due to the lack of one of the levels not regulating the input.
  • These DON’T regenerate!
  • The A-fibers then begin to grow more and now light touch becomes an issue leading to difficulty with discrimination of your left/right sides.
    • Mirror therapy!

The Brain:

  • There is no pain area in the brain!
  • Some common areas light up but the pain experience is a combination of multiple inputs from multiple areas of the brain.
  • On brain imaging from fMRI, chronic pain patients have a brain that is very alert and hyperaware. There is too much going on! If our goal is herniated disc -> pelvic tilt -> and we make them think that they have to maintain this all we are doing is increasing input to the system that is already overloaded
    • On a side note: chronic pain and abdominal exercises. No, they usually aren’t “weak” but actually they are already co-contracting too much. If we focus on this even more then all we are doing is scaring the patient into thinking that they are too weak and this will increase the system even more! We need to down regulate!
  • Typical Pain Nueromatrix taken from A. Louw (these are the areas that light up the most)
    • Premotor cortex/motor cortex
      • Movement
    • Cingulate cortex
      • Concentration and “fog”
    • Prefrontal cortex
      • Memory
    • Amygdala
      • Fear and addiction
    • Sensory cortex
      • Right and left discrimination, joint position
    • Hypothalamus/thalamus
      • Stress responses, chemical output and motivation
    • Cerebellum
      • Movement and fine motor control (ie. Those patients who can’t even perform those simple lift leg up exercise)
    • Hippocampus
      • Fear conditioning
    • Spinal cord
      • Peripheral inputs
    • As you can see from the above list, increased input from the spinal cord influences all of these areas. Think about your patients who are too tired to get out of bed, who are too fearful to move, lack motivation, have a difficult time even with simple tasks, etc
    • If a patient has difficulty with simple tasks because the brain is too active and that area has such a low threshold. The communication between the brain and the body is impaired. This can lead to those imbalances and poor movement that we see.
      • Not necessary weak but rather inability for brain to focus on that one specific movement

The output:

  • The brain puts every other system on hold except for the most important ones. It decides this based upon threats. If one threat is larger than another then this system will take precedence.
  • The brain releases a whole host of chemicals in response to the perception of a threat/pain
    • Adrenaline
      • Stress chemical (see below)
    • Cortisol
      • Shunts blood and can make tissues sore/tired/sensitive/fatigued
      • Impacts sleep, memory, concentration
      • Increases nerve sensitization (ion channels), persistent inflammation (makes the body think that an area is still injured when not thereby increasing sensitivity to an area), and general malaise.

In summary:

Once you understand that the brain controls everything. Questions begin to answer themselves. For instance, general “patella femoral” knee pain. We can all agree that the research shows an impaired onset of the activation of the VMO versus the other quad muscles. But why? Well, if you believe that the brain truly runs the system, then you have to believe that there is a reason for it. Not because there is pain there. Pain is not there! Pain is in the brain! So if you have someone that collapses in with running and there medial knee is painful with a reduced VMO activation (we can’t measure this in clinic). Then look further. If there is a dynamic valgus then the patella no longer needs to track medially. It make sense for the patella to stay in the groove and this would be best accomplished by activating the vastus lateralis first. The problem would be at the hips and proper control over the musculature in that area. This does NOT include just SLR 4 way and call it a day but much more.

If everything is regulated by the brain then so is manual therapy! Yes, we like to think that we are doing this awesome adjustment. But really all we are doing to sending a neurological feedback into the system which hopes to “reset” the system. At least give us a way in. Watch the Medbridge Chad Cook cervical lecture and he points to some great research showing the chemical effects that manual therapy has and the short time effects if it.  I will also go into how to explain it to patients (creating handouts soon) and also what this means in respect to different cases and “painful” experiences.

Disclaimer:

I really like to use pain science to better understand what we do as therapists. But it should never be used alone. There is always something we can do to help the patient. Use reset systems (like Mackenzie, mulligans, any manual therapy), use proper words and also improve movements. Give the patient hope and a purpose to getting better.

~ TJ Slowik

Thank you to Adriaan Louw for one of the best continuing courses I have taken (through medbridge).

Thank you to Adriaan Louw for one of the best continuing courses I have taken (through medbridge).

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Pain Science: Part 1…

Pain Science Part 1

Pain science is a topic that I really wanted to discuss since I started this blog. Much of what I do nowadays refers back to pain. Our job as therapist is to treat patients who are in pain. It is what we do. It is why we get paid. The end product of every patient that walks through that door is to relieve their pain and to improve function. They are dependent on each other. Do you really think that a patient will be happy with the care if there is not a pain reduction? Probably not even if they can function normally. They came to us to help their pain. Then why do most therapists not know what pain is? Where pain comes from? Many therapists, and I did for a long time, feed into pain. We give it life. We make it worst with our words and demeanor. I hope that, at the least, what you can take away from this is to not feed into the pain. To debunk the common myths about pain so that you can communicate that to your patients.

Pain education isn’t only important for chronic pain but also for acute pain. All pain does start at some point. Hopefully, if we can educate our patients early on in the process we can begin to change the onset of chronic pain. Take a patient, who may be at risk for developing chronic pain (many reasons for this), and help to reduce the effect that pain has on their future self. Like most other “interventions” it is not best to memorize the information but rather to learn the concept. You can apply an intervention to a handful of patients but you can apply a concept to every patient. Learn the concepts of what pain is and what pain isn’t. Learn how to properly explain pain to patients. It changed my career path and I hope by at least starting this conversation with you that it will do the same.

There are many avenues to learn more about pain. The first is research of course though it is harder to find in the US versus other countries who push out a lot of research about pain (if looking for research just look at Moseley and all the research that he puts out). The US seems to be focused on this drop step/jump down and rehashing old and abused research material. Honestly, do we need another research article on a step down task or jumping tasks to know that faulty mechanics equal ACL tears/other injuries? What we need is more research on the rehab behind this and proper exercises that will improve this functionally and not the same old 4 way SLR with some planks thrown in for good measure. The second area that I have learned the most from and is where much of this talk comes from is Medbridge course by Adriaan Louw called “teaching people about pain”. If watching this course doesn’t completely change your practice re-watch it and really try to learn the concept. Not the individual parts. Thirdly, are the blogs. In the margin I have a lot of blogs that I follow. All experts and clinicians that I admire. If I become half the therapist that they are my career will be a success. Some of the ones that I like the most for pain:

  • Noijam and
  • Body in Mind.
  • Forward Thinking PT
  • Explain Pain

Yet, all of them have some type of pain related education involved in their postings.

So why is pain science important?

Chronic pain has doubled in the last 15 years and continues to be a growing problem in the clinic. Chronic pain itself can be hard to define but for simplicity we can give it a quick definition of pain that the patient is perceiving that has lasted longer than the healing phase for the original acute injury (though ~ 30% of chronic pain doesn’t have a related injury). Treating chronic back pain isn’t always about targeting core musculature or activating the TA or giving heat/stim and “cracking” them. It starts way before any intervention that you want to give. You must treat their fear and beliefs first.

Fear can be defined as a distressing negative sensation induced by a perceived threat. The fear of pain is worse than the fear itself. The circle of fear is something like (from Vlaeyen, Linton 2000)

Injury -> Pain experience -> no fear -> confrontation -> Recovery OR

Injury -> Pain experience -> Fear from lack of knowledge/medical tests/words/internet -> Pain catastrophizing (irrational thoughts) -> pain related fear -> avoidance -> depression/anxiety to move/disability -> feeds back to the pain experience again.

This is where we need to educate them and stop that second loop from starting acutely or move them out of the second loop.

Many patients in pain have impaired beliefs about pain such as:

  • Pain is always bad and pain equals injury
  • All pain must be gone before engaging in normal activity and movements
  • Pain will increase with all activity/any activity
  • Passive treatment is the best
  • I have to live with pain the rest of my life

We feed into these beliefs by using our words. These words include any medical test findings such as arthritis and bulging discs, something is out of place, your posture is bad therefore you will have pain, you have a weak core or you are “unstable”. I am not saying that some of these don’t happen or that we shouldn’t treat what we see as deficits but rather we need to pick our words better. They are very abrasive words and telling someone who sits all day that there posture is causing their pain then that will only increase the hyperactivity of the entire system every time they sit!

Our educational systems feed into these beliefs as well. It is hard to change something that you learned in school and then practiced when you graduated. It is not easy to start to change your thinking. Believe me, I know! It is a small steps each day to change the way you think about pain and change the way your patients think about pain. It is hard to drop this biomechanical model/patho-anatomy model of pain in lieu of something that you can’t see! Once again, I am not saying to drop the entire system and only think about pain. That is not at all. But question what you have been taught and why things happen. I use the biomechanical model with pain science to explain the reasons why the brain could be perceiving outputs as pain or to explain the original injury. I am very much biomechanical based but adding pain to the whole picture actually clears up so any questions that I have. [Look at “explanatory and diagnostic labels and perceived prognosis in chronic low back pain” by Sloan/Walsh 2010 Spine.]

Definition of pain: “Pain is a multiple system output, activated by the brain based on a perceived threat” (Moseley via Louw)

Lorimer Moseley performed a study on someone with 4.5 years of pain. Pain started as LBP then became widespread in lower extremities. Using an fMRI they measured brain level activity. On evaluation the fMRI showed severe hyperactivity of the brain. Then they educated on spinal stabilization exercises for one week. There were improvements! But mild! There was a small change in hyperactivity of the fMRI. Then they educated patient for 1 session on pain and did nothing else. What happened? Severe decreases in brain activity. Pain education decreased pain much more than any spinal stabilization exercises. I know that it was just a single subject but isn’t that enough to warrant a longer look at it. [Moseley 2005. Widespread brain activity during an abdominal task markedly reduced after pain physiology education]

There are more: A couple of systematic reviews on therapeutic neuroscience education from Clark and Louw that also show marked improvements in chronic pain. Lorimer Moseley/Body in Mind have plenty of articles to keep you busy.

Tissues and pain

  • Tissues due to get injured! But they heal!
    • And even shown that disc bulges reabsorb in one year.
  • Tissue injury does not equal pain
    • I have read anywhere between 40- 60 % of people have a disc bulge with no pain
  • Arthritis does not equal pain
    • Arthritis is one of those bad words. Patients feel doomed by the thought of having arthritis and become afraid to move. How terrible that is. The one thing that will help them they become afraid to do inciting a hyperactivity throughout there CNS.
  • Cool study on “neck pain in demolition derby drivers (Simotas, Shen. 2005)”
    • Shows only a 2.5% chronic neck pain
  • Shoulder after rotator cuff repair. MRI imaging findings in asymptomatic individuals (Speilmann 1999)
    • 90% showed abnormal signaling and 16% had partial tears while 20% had complete tears

In my next post I want to go through the pain process. How pain develops and where it comes from. I am going to review the basics from what I have learned.  I have many more research articles which I think that I am going to review as a group after the next post.

Final thoughts:

Like I said above, and I want to reiterate. I know, that in order to treat patients, we need to look everywhere for the possible reasons why someone is in pain. Sometimes it is simply fixing the mechanics to take pressure of an area. Yet, it is also, fix the mechanics to take the pressure off an area and have a neurological input that decreases the hypersensitivity of the nervous system/brain. Think more! Challenge yourselves to go above the standard treatments for people in pain. Remember: we go to work and then leave work but patients come to clinic in pain then go home and there pain continues. For many of our patients the pain never ends. Think about that! Pain that never goes away. Think of a time that you had pain from an activity (as most PTs were athletes at some time we all have them) now think about it being there all the time and every day for years. That is what many of your patients experience.

~ TJ

Follow up: Case Study: Cervical pain post concussion

Follow up to Case study: cervical pain post concussion

I treated patient on 11/13 two days after the initial evaluation. Patient reported that her neck pain and movement was a lot better and working on HEP throughout day including at school. She continues to have no headaches or dizziness. Her major complaint now is with sidebending and lack of activity. She really wants to be ready for indoor soccer season which starts in a couple weeks.

Re-check of measurements:

  • Bilateral Rotation and sagittal AROM of cervical remains full and only a 1/10 pain (in upper traps)
  • Her cervical retractions look great and can repeat without incident
  • Thoracic rotation actively is good
  • Upper trap spasms continue but subjective report of much improvement and no more medial scapular border pain
  • Sidebending is limited to about 50% of max (she has a long slender neck and should get a lot of motion in this directions) and has moderate pain

Treatment

  • C-T distraction again
  • IASTM to upper traps and cervical paraspinals
  • Weight bearing cervical retraction with sidebending
    • Reported a lot of pain and was apprehensive to continuing
  • Non-weight bearing cervical retraction with sidebending
    • Tolerated much better and performed until able to get what looks like full PROM
  • Revisited the weight bearing cervical retraction with sidebending
    • Able to tolerate now and improves her motion and pain but still not full AROM that she had passively and pain is still present.
  • Supine mobilizations of cervical segments (right to left and left to right)
    • Moved into more closing with reps
    • Rechecked AROM sidebending and now improved and only mild pain to perform
  • Attempted Upper rib manipulation to left side to reduce upper trap spams but unable to get a good lock and no cavitation. Did on right side and same result
  • Bike, bird dogs, mid/low trap (T/Ys), planks and squats
    • Performed some mild exertion activities to increase blood flow and to begin exertion training for return to sports.
    • No neck pain and no concussion symptoms throughout this part of the program
  • HEP:
    • Same as previous, added the exertion components listed above, cervical retraction with sidebending and also gave a towel pull (isometric horizontal abduction) with row.
    • The towel pull with row seems to get some scapular retraction without flaring up the upper traps

What could I have done different? What would you have done differently?

Any advice on the sidebending? Any advice on upper trap/cervical spasm reduction?

What would you give next visit?

Case Study: cervical pain post concussion

Case Study: cervical pain post concussion

Meant to post this earlier in the week once I saw the patient then update it after seeing her for a second time. Here is the original evaluation then the follow up is at the end of the post.

On 11/11 I had an eval for cervical pain post concussion/whiplash. Prior to seeing the patient I talked to our vestibular therapist to give me an update on her. She was highly symptomatic (headaches/dizziness) last week but today she was doing well with no complaints of headaches or dizziness. The most glaring issue was that she was unable to test any head thrust and VOR measures due to the lack of cervical rotation due to pain.

Subject:

  • High school female soccer (outdoor and indoor) and track athlete.

Past medical history:

  • No prior concussions or neck injuries. Did have bilateral hip pain last year during soccer season but did not have any pain this season.

Incident:

  • Was elbowed in head during a soccer game in the middle of October. Initial symptoms consisted of headaches, dizziness, concentration difficulties and fogginess.

Subjective history of current events:

  • Started having neck pain a couple days after concussion and was in vestibular two weeks after the incident. After first visit vestibular therapist referred her to ortho to address neck pain and to get full AROM so that they could progress on with therapy. She missed the first eval and wasn’t able to get in to see me until 11/11.
  • The pain is constant and gets worse as the day goes on. Hasn’t been involved in any sporting activities or working out due to the concussion. No headaches now so unrelated to neck pain currently though she did report that the neck pain would go up and give her headaches previous to this week.

The initial evaluation:

  • Pain
    • Pain is moderate at rest and severe with cervical AROM
    • Pain centralized to bilateral upper traps and down middle of cervical spine radiating out to the medial bilateral scapular regions
  • Cervical AROM
    • Right/left rotation = 32 degrees with increased pain (severe) on both sides of neck and upper traps
    • Sagittal = 60 degrees with increased pain in both directions (same areas/intensity)
    • Sidebending is restricted to left= 24 and right = 20 with severe pain as well
  • Tenderness (for completeness)
    • Upper traps, sub-occipitals, cervical paraspinals, medial scapular soft tissue and in the thoracic/cervical with P-A over the spinous processes.
  • Strength:
    • Normal shoulder strength and no myotomal weakness
    • Mid/low traps= 3/5, rhomboids= 4+/5
  • PROM
    • Full flexion/extension in supine.
    • Left/right rotations limited due to severe pain but able to get about 75 degrees
    • Sidebending to 45 degrees with severe pain limiting motions
  • The AROM restrictions of O-A, mid cervical vs lower cervical are limited due to the pain
  • Spasms and blocks movement with attempts at any sideglides to cervical region

Treatment

  • PT assisted Non-weight bearing (supine) Mackenzie exercises for extension
    • This includes:
      • Traction with retraction (5 reps) then moved straight into traction- retraction- extension followed by nodding maneuver at end range extension
    • Response:
      • Increased pain with first rep but no red lights -> finished 10 reps
    • I performed to gain extension which often times helps all motions as well. Probably more of a neurological feedback than actually placing anything into proper alignment (helps to decrease apprehension of tissues blocking movement?)
    • Once sitting I re-check motions and had improved flexion/extension greatest but pain at end ranges still. Mild improvements in rotation and pain.
  • Performed C-T distraction and audible cavitation (patient was not impressed! Haha)
    • Improved flexion to near end range with decreases in pain with both flex/ext
  • Weight bearing Mackenzie exercises for extension
    • 10 reps of cervical retraction
    • 10 reps of overpressure
    • 10 reps of retraction- overpressure- extension with nod
    • Full extension now with only mild pain and less upper trap spasms/scapular pain
  • Instrument assisted Soft tissue to upper traps and cervical paraspinals bilateral
    • About 75 degrees of rotation, sidebending is improved but still an issue with pain
    • Reduced spasms quite a bit through cervical region/upper traps
    • I choose to use IASTM vs trigger point releases because…
      • What are trigger points?
      • Seen much better results in session and sustained with follow ups
  • Final: Horizontal abduction pull on theraband with cervical AROM in all plans
    • Just 8 reps of rotation to each side, flexion and extension
    • Full rotation bilateral now with only mild pain at the endranges. Extension and flexion is full and only a 1/10 pain.
  •  HEP:
    • Weight bearing Mackenzie extension exercises
    • Horizontal abduction pull with AROM
    • Weight-bearing thoracic rotation exercise with band pull (was restricted and now full thoracic rotation)
    • Bilateral External rotation with retraction and breathing
    • Patient was finally impressed at the end of the session when she could rotate her head for the first time in weeks.
  • Final thoughts:
    • I always like going NWB manual Mackenzie exercises to start. I feel like it helps the patient adjust more by putting it in my hands vs their own. I always try to finish with HEP weight bearing though.
    • Love IASTM to cervical region for reduction of “spasms”. In my experience the carry over for improvements if you follow it up with the band pull with AROM and Mackenzie exercises is very good.
    • In previous post I love the band pull with AROM when there is a clear limitation in AROM vs PROM. Helps to improve a lot of things including thoracic rotations.

Rolling…yeah I roll

Rolling…rolling…really? This is something that I have done enough times that I have seen great responses with. It has a purpose and if done and followed through with can be very beneficial. Even though I have done this several times I still continue to get questions and stares in clinic from both physical therapists, students and patients.

When do you decide to roll?

In the SFMA course that I took, the instructor (Greg Rose DC) referred to it as turning the switch on. For whatever reason, your “switch” has been turned off and we need to turn it back on. This “switch” is the motor control switch. Usually, in more chronic or longer lasting issues (pain or faulty movement patterns) there is this global motor control issue.

So, when you test functional movements and then break it down into individual segments there are many deficits. Each time you test a passive vs active ROM there is this overwhelming amount of full PROM and limited AROM. Also, the AROM looks “dirty” as in they compensate greatly to achieve a desired outcome. I will test rolling when someone has asymmetrical global weakness (such as in the hips or shoulder), when they show me poor movement patterns in deep squat/backward bend/full body rotation/lumbar flexion and/or they can’t activate their glutes (with prone hip extension they say they feel it in their hamstrings and/or they have a lot of compensations to get the leg smoothly up).

Why do you roll?

It is actually quite simple. If someone can’t roll correctly then how can they possibly perform exercises in any other position such as half/tall kneeling and standing? The way we develop, we start by rolling and then crawling then standing. We can’t skip steps!

The reason why we can’t roll?

I really think, from seeing the patients who fail at it, that we develop faulty movement patterns over the course of time. This could be a result of a previous injury years ago, our very sedentary lifestyles/jobs or the result of our chosen sport. The longer we go with a poor movement pattern then the more engrained into our nervous system that pattern becomes. Rolling is just the first step.

How do you test rolling?

There are four quadrants in both supine and in prone. I usually start in supine. You want to move one body part only and attempt to roll using that one body part. If you are going to use the upper body then the lower body is paralyzed and not allowed to help at all. If there is any activation then that attempt doesn’t count and they should redo it. The patient has to be honest with you and usually after seeing a couple good movements then most times you can see the compensation. Once the upper body is tested in supine then you test the lower body when the upper body is paralyzed.

Supine right shoulder flexion -> supine right leg flexion -> supine left shoulder flexion -> supine left leg flexion

Prone right shoulder extension -> prone right hip extension -> prone left shoulder extension -> prone left hip extension.

How do you treat rolling?

Most often times you will see one area that is especially dysfunctional though there may be multiple areas that need to be worked on. Say the right hip extension is dysfunctional. In order to treat that (this way is easier so that they can replicate it at home versus using a sport cord) dysfunction you place a pillow under there right hip/torso (decreases difficulty by 25%). If they still can’t do this properly you add another pillow to make it 50% easier and so on until they can easily roll.

Once they accomplish the rolling task with, let’s say two pillows, then you want to take one pillow out and make them work for the 25%. Once they pass a step I would make them do a bunch of reps first before increasing the difficulty. Do this at each stage until they are able to roll successfully from the floor.

What can it help clear up?

Remember, whenever you want to make a quick fix always have that movement or test that they failed and retest after they perform the intervention to see if it helped clear anything up. So, if they failed prone hip extension because of both poor active ROM and excessive hamstring activation then you want to go back to that test and see if it is better. It may not be an excellent grade after but you should see a considerable change. This change should be enough to allow you the “in” to start working on those individual motor control deficits.

Sometimes over the course of the session they still aren’t able to roll without assistance. That is okay! That would be there HEP and to progress to the floor. You can give a few small, simple motor control exercises after rolling but I would make their HEP following their initial evaluation focused on the rolling. The changes should maintain and stay as long as they are consistent with working on the movement at home. Most likely these patients will have a lot of deficits to slowly work on because their entire system has been shut off for so long. Those inhibitory muscles, overtime, can become actually weak as well.

What patients will this help?

Most athletes and people who have sedentary jobs where that extension mechanism is just lost. Chronic pain patients where the general programs just haven’t work to decrease their pain or improve their function.

Runners: usually their injuries are a lack/loss of active hip extension when running. This hip extension needs to be from the glutes and not the hamstrings or lower back. Ankle injuries/shin splints fall in line with this as well. Activate the glutes and entire posterior chain extension mechanism.

Swimmers: who have been using their shoulders/neck/lower back and hamstrings for long periods in the water will sometimes just need that relearning of proper muscle activation to go with all that motion.

Baseball players: Like swimmers, upper/lower body sports require better movement patterns

Golfers: they lose that motor control with rotations which can translate up/down the chain

Flexion based activities: just because they can’t reach down and touch their toes doesn’t mean tight hamstrings or lack of mobility. Often times they have impaired whole body movement patterns.

Questions…?

TJ Slowik PT DPT

Active Vs Passive ROM (Cervical Spine)

Active VS Passive ROM (Cervical)

This is my first post relating to active vs passive ROM testing and treatments. I want to start in the cervical region.

One thing that I noticed going through school and then as a floater and now as a clinical instructor is how little therapists respect the great knowledge that you can gain by knowing the difference between active and passive ROM. Many, if not all, therapists check active/passive ROM of the shoulder. We mobes/PROM shoulders that have restrictions in both. If just active is limited but passive is full then we work on correcting the deficits in shoulder strength/control. Why don’t we take this into account throughout the rest of the body?

In school and in practice I see many people using the cervical ROM diagram. It allows us to easily list ROM, pain, stretching, radicular symptoms, etc. in one easy to find/use space. It works well and acts as a quick reference for busy times. The problem is: why is there only one of these on most initial evals? There should be one for active AND one for passive ROM. When one of these diagrams looks like the following:

pain diagram

Then we assume (as manual therapists) that there is a closing restriction on the right side. We then put them supine and check each individual segment for mobility and pain. I don’t want this to turn into a discussion of our palpation skills. That can be saved for another time. In short, they are not good. Have you seen a cadaver?

If AROM is limited in all planes or just one plane but passive ROM is full then we really need to start thinking motor control! If AROM and Passive ROM are both restricted then we do need to asses to see where that restriction is coming from. This passive restriction can have many components and that is where we use our heavily developed manual skills to address then retest and check for improvements. Most times, if there is a passive restriction to motion and you clear that up with manual therapy then there is usually a motor control deficit to follow when you re-test the AROM and PROM. Also, don’t just check that first day but rather continue to check the Active vs Passive ROM.

Passive ROM restrictions is a result of something. It doesn’t just happen (like hamstring tightness which is a very long future post). Often times, if you fix that passive restriction they may have full AROM right after as well. This doesn’t mean that there isn’t a motor control issue to address. This change in AROM can be a result of the neurological feedback that you get with manual therapy. It can help reset the system including the active restraints to motion. Re-test the PROM/AROM the next visit to make sure that the PROM remained. If it didn’t then suspect a motor control issue that is preventing motion on continual basis. Follow your manual therapy up with some motor control exercises and see what happens the next visit. If they are consistent with their HEP then there should be those lasting changes.

When I first started thinking of adding more motor control exercises (opposed to the usual row/shoulder/scapular therex) into my treatment plan I was skeptical that it would carry over from one treatment to the next. Once I saw the results I was excited. I always question how we can be better at treating patients and the thought processes behind certain treatments. If PROM is full and AROM of the cervical region is limited then how can I regain full/painless AROM?

I hear a lot of experts talk about the reasons why we aren’t great at treating patients and areas that we need to improve upon. In the SFMA course I took over the summer (the philosophy behind there treatments pretty much changed the way I treat) they had mentioned that diagnosis is the area that we struggle in the most and that we are passible with the interventions. I don’t disagree with that assessment. We struggle with the “real” diagnosis with many patients, that is, in regards to what are focus should be on. But, I also think we really struggle with our treatments. This includes doing too much, not enough, poor progression, targeting the wrong areas, etc.

The big area that we struggle in regards to treatments is wanting to strength train everyone. Motor control is a huge component of a lot of areas and compensations. This is a talk for maybe my next post and many, many posts after that. For now, let’s talk about just improving that cervical AROM. In some ways I don’t even care what is limiting AROM. AROM involves contractile movements as well as non-contractile structures. If PROM is free and clear then what is more of a concern to me is how I can access that motor control system or nervous system.

It isn’t about strengthening the muscles or stretching non-stop to restore motion but rather about the amount of inactivation that is occurring. The motor control system just isn’t working. Overtime, the patient, somehow, developed a poor movement pattern. This poor movement pattern is possibly a result of a poor nervous system activation. It is not strength! You can do all the muscular strengthening and upper trap stretching you want but if you can’t get the system to respond normally then there will not be lasting changes. The body is a system of nerves, nervous system firing and brain mapping that churns out a desired response.

Try going weight bearing first and then if they can’t complete the below exercises go to supine and work on first.

Pull a thera-band apart into shoulder horizontal abduction with both hands and then have the patient actively rotate their head to the left then right. Once finished with that have the patient relax the band back to a relaxed state. Repeat ten times. Then do the same with any other motion that is restricted.

Horizontalabductionpull

You should see an instant improvement in AROM. It will look cleaner, be less painful and the patient should also instantly see/feel the results. I am not saying that it will be pain-free but there should be a noticeable difference in pain levels as well as AROM. If they are still painful then try some sustained overpressure with movement (at some level of the cervical spine from posterior) while they complete the above exercise. This can provide a little neurological feedback to the system and help with the perception of pain.

There is no one definition of motor control or what happens/why we see altered movement patterns when there is pain present. Why/how the nervous system goes about its processes is poorly understood and needs a lot more research focused on this. Hodges and Tucker have a good article on this process in 2011 (see below). A possible mechanism could be through the nervous system. If we can activate a “core” muscular group such as the scapular stabilizers in the upper quarter then maybe this will feedforward. The goal of this exercise is to get the CNS firing first then performing the abnormal movement hoping that it restores the correct timing/coordination of muscles thereby reducing the perception of pain.

Remember this is just one way of improving that active ROM and should be combined with other techniques and ways to reduce the hyperactivity of the nervous systems in through the cervical region. I will only quickly mention the couple other ways that I use as well but save for another post.

Mackenzie extension (clean up PROM/AROM)

Instrument assisted soft tissue massage to the cervical region (neurological feedback not scar tissue!)

Nerve tensioning/slides/glides/release via David Butler

I intend on going through the rest of my cervical treatment interventions to decrease pain and increase ROM as well as increasing function in following posts. I believe that it is very important to know why you perform the interventions as opposed to just assigning interventions because “you have always done it like that”. My interventions and treatment strategies have changed a lot over time and it is because I am trying to constantly look for ways to improve my outcomes and question the norm.

TJ Slowik PT DPT

Hodges, P.W., Tucker (2011). Moving differently in pain: A new theory to explain the adaptation to pain.

Hodges, P.W (2011). Pain and Motor Control: From laboratory to rehabilitation.

Changing Conventional Thought

Changing conventional thought

My first real post on here was originally going to be reserved for pain or maybe motor control and inhibition/compensation seen in runners/athletes of all types since I have seen a few more of those patients recently. But, now I just want to talk about being a physical therapist for a moment.

Over the previous 6 months my treatment principles have undergone a major transformation. You tend to realize the things that you don’t know or don’t have a good answer for when you have a student. Wanting to educate the student and really increase their level of understanding comes first from your understanding what is going on. This extends to the treatment of the patient. The why questions pop up a lot and I hate not having a good answer for them or at least a possible reason. I always had a lot of questions and attempted to answer them for myself but something about being partially responsible for a future physical therapist really motivates me.

This week a new student started with me. Today we talked a lot about pain and the the difference between motor control and strength/core stability. Going through the explanations of everything made me really think back to this whole changing a young therapists mindset and how much different it is to think along these lines vs what you are taught in school. I just graduated about a year and a half ago and for the most part the information being taught hasn’t changed much. ROM/MMT/flexibility and biomechanical changes in joint positioning. These were the things that were heavily stressed to be important. What wasn’t stressed was how meaningless all these are. Humor me for a second.

ROM: Yes, A/PROM is very important but it is amazing at how little so many therapists take into account active vs passive ROM in the spine. Just because lumbar flexion is limited in standing doesn’t mean that the hamstrings are tight or there is a joint that is out of place. You have to check passive as well in an unloaded position. What is worse is the cervical region. Limitation in ROM sitting does NOT mean that there is a closing/opening restriction. You have to check PROM in NWB. Most times this motion is actually perfectly fine and it is not something you need to start closing down or manipulating telling the patient that they have something out of place. All this does is raise their pain avoidance levels.

MMT: Please don’t rate someone a 4/5 via MMT of hip extension if they can’t complete AROM of hip extension without hamstring compensation. That 4/5 in glutes quickly turns into a 4/5 in hamstring strength and less than a 3/5 in glutes. Also, strength, most times means nothing if they can’t use it properly.

Flexibility: Tight hamstrings? The cause of Pain? Really? Come on. Just ask yourself this question. Why does something get tight? It a protective reflex from the CNS. You have the find the cause/movement dysfunction that is causing this massive compensation.

Manipulation changes joint mechanics: Where have you ever read that palpation skills are good? Have you ever seen a cadaver? If you manipulate something that isn’t out of place do you make it out of place? So how is it that manipulating something returns it back into place? Most research shows that it is impossible to target a specific joint without getting residual movement in surrounding areas so how can you really say that you are only manipulating the SI/C6/L4 etc.? Yes, manipulate and mobe but know why you are doing it so that you don’t scare the patient into believing that they will fall apart if they rotate slightly.

I know that I took the above to the extremes and there are always exceptions but for the majority the above is very much true.

This got completely off track quickly.

I faced the above reality when I stopped thinking about conventional PT treatments (cough, any doctor TV show, cough) and began to look at the body like we should. This includes less about strength/ROM and more about movement patterns and inhibition. Less about core stability and more about what pain is and what it isn’t. It is difficult to reboot much of what you have learned and takes time to really get back into a comfortable treatment approach incorporating all the new information you learned especially with major changes being made.

With a new student, I realized that I am still learning how to incorporate these new philosophies into my evaluation and treatment processes. It isn’t engrained into my thinking patterns yet but, like motor control/inhibition, practice will help write that new book.

Signed…the always honest TJ