").appendTo("body"); });

Why aren’t we turning the light switch off more in rehabilitation?

Why aren’t we turning the light switch off more?

Lightswitch.png

 

Remember the Clapper?  “Catchy jingle” is how Morgan Freeman described it in Bruce Almighty.  A simple device applied to a light switch that is designed to turn the light on or off when a clapping of the hands happens.  Super popular in the 90’s. “Clap on…Clap off….the Clapper”. Got me thinking after I saw that the clapper was still available for purchase…what if…as rehabilitation professionals we were able to turn off a client’s symptoms during their visit instead of producing them?  What if…we were able to do that and then show the client how to reproduce that themselves?  Now I’m not talking about avoiding pain.  I’m not even talking about talking it easy on our clients in rehab sessions by not having them work hard or achieve muscular fatigue during exercise.  But rather, I’m suggesting, that as part of an assessment tool, we try to determine if the use of forces around the body with our hand, education, postural changes, belts, etc, can turn the symptom ‘off’ instead of ‘on’.  What information would that give us if we could do that?  With all the social media ‘disruptors’ and challengers out there (nothing wrong with it), it seems like we’re being convinced that we haven’t gotten ANYONE better in the past 50 years!  Successes that we have seen appear to be merely a fog curtain of Hawthorne effects and placebos. Our biggest challenge in healthcare is NOT the mechanisms of how we get people better.  Not even the application to get to the mechanism.  Our biggest challenge is the clinical thought process of why we do what we do!  In 17 years as a physio, I’ve gone through the doldrums of success and failure.  I’ve convinced myself that I was top of the food chain, and sweated the disbelief of letting my patients down of not achieving their goals. 

One of my biggest epiphany however came from the realization that I could get just as much (if not more information) about my patient from attempting to eliminate their symptoms alongside trying to stimulate them.  @Keyclinicalskills refers to this as “Light switch off”.  By turning my attention away from “does this hurt”, “ooooo this feels restricted” and the ever loved “this end-feel feels tight”, and focusing on “do your symptoms change when I do this?”.  Recently published studies have even demonstrated dramatic changes in cerebral processing are being seen with fMRI just by changing the words we use and the focus we place on movement (found here).  I have found several things have happened when I attempt light switch off testing and treatment.  1) I automatically engage the patient! Positively! Establishing a therapeutic alliance is becoming more documented in the literature and is defined as the working rapport or positive social connection between the patient and the therapist 

 (found here).  2) Buy in from the patient.  We have established our profession as the “Physical Torturists” or “Personal Terrorist”.  All lovely titles! From the outset of rehabilitation in the physical therapy setting, some people are automatically expecting pain when they come in for their visit.  “Just do what you have to do” resonates throughout clinics across the globe as we have convinced people the only way to get better is through trial by fire and pain! Why is this?  Are we finding justification through experience and research that lightly suggests that painful treatment are better than non?  Have we given up on the possibility that turning off pain could lead to normalcy? 

Now this suggestion, while logical, is a huge uphill battle.  I cannot remember any aspect of learning how to look for pain free objective signs in PT.  My education, both during schooling, and in most of my 574 hours of post-graduate continuing education since has been focused around pain producing special tests. 

Problem?  Chad Cook and Eric Hedeges would argue yes! 

Chad and Eric have authored 2 different documents that are leading our profession to question what we are even looking at with our ‘special tests’.  One is Orthopedic Special Tests Volume 2 and the other is an opinion piece published in JOPST earlier this year (2017).  The over-simplified conclusion?  We have fooled ourselves with biased research and a misunderstanding of previously conducted studies that have yielded and abundance of unreliable special test…that aren’t that special!

Are we clinging to old perceptions of evaluation and treatment?

Are we clinging to old perceptions of evaluation and treatment?

So back to my early statements.  What kind of value could be place on performing tests that were designed to eliminated symptoms instead of producing them?  I have established a habit over the last several years of attempting forms of pain-eliminating tests first to determine results, then returning to the pain-producing testing after to compared notes. 

Something interesting that I have found from symptom-eliminating testing is the response from the patient.  Case in point, imagine the painful knee patient who has already been told that they have advanced arthritis in their knee and that portions of their meniscus are torn after MRI.  Often, they are unsure as to why they are in therapy because their condition cannot change and their beliefs have been established from a consult from a healthcare professional who has not educated them on pain or the research findings that knee OA does not equal pain and dysfunction for every person.  If I perform painful special tests on them in an attempt to produce pain or limitations first, I often justify to them their beliefs of the problem or issue.  Now, what if I attempt the opposite.  What if Mrs. Jones is a responder to improved pain-free ROM and function with simple forces applied across her joint line while she performs that actions that she describes at limiting?  “What happened to my OA?” is the most common response I get. “Exactly my point. Nothing happened to your OA Mrs. Jones.  But now we know that your body has the capability to operative without that limitation.  So now we just have to figure out how to make that change permanent.”  Moving toward a complimentary team effort with my patient about what means the most to them and away from fully passive treatments has made it easier to establish patient empowerment and control over their symptoms.  People feel listened to. 2) If symptoms can be altered, and preferable abolished, it automatically begins that question of “If I can move without that pain or restriction now, what happened to my “X” (insert OA, tear, degeneration, posture, etc) diagnosis?”.  The transition from a diagnosis to Pain Neuro Science (PNE) happens seamlessly. Beginning to understand that the vast majority of symptoms that we see clinically in an outpatient setting fall under the category of “top down”.

Imagine a world where you were above to move and function without pain?!?  Yeah…it’s called normal!

Lightswitch3.png

It may be easily argued that the Therapeutic Alliance has already begun in this scenario.  The patient would likely “buy in” to the treatment approach quickly with a positive response.  Especially compared to the more traditional approach of “light switch on” special testing and treatment. But “light switch on” not only does have value proven in the literature (see cross over leg raise example here), but working with pain can have its advantages as well.  I often have my clients focus on the pain that they are having and determine what happens to their pain when they move or exercise.  “Ok.  Let’s see what happens to your pain or limitation if you do more repetitions?  Is it getting worse, better, or staying the same the more you do?  I classically get even more information after a bout of painful exercise or movements…”now let’s try that again and tell me what has happened to that pain you were reporting earlier.”

Unfortunately, while there have been countless observations in the literature of these types of treatments (see here), to my knowledge there have not been any performed directly related to specific conditions.  But do we really need specific research to perform “light switch off” testing?  Can we really infer that a sub-group of responders would give any value over an N of 1? 

Perhaps we have given the painful approach too much credence over time.  Have we relied on special tests and painful treatments to define who we are as a profession?  Maybe. Is it time for a paradigm shift in how we conduct an exam and treatment and start including pain-free testing and treatment?  Maybe it’s time to consider both pain free manual therapy and pain free exercise.  And if we can do that, then LOAD IT!  Load it heavy, and often, with current suggestions from Prof. Jill Cook among others. 

Thanks for reading.  Now that you're done, turn off the light please!

Eric

Motion Guidance

Whiplash

I wonder if head-bangers report less pain and dysfunction after an MVI? 

I wonder if head-bangers report less pain and dysfunction after an MVI? 

W.A.D.

Whiplash, known to practitioners as “WAD” or Whiplash Associative Disorder, is a collection of symptoms associated with a specific traumatic onset. If you are familiar with rehabbing this cohort, you’ll know that symptoms tend to be more chronic in nature, and it is a condition that tends to respond differently than the typical mechanical neck pain patient.

This blog will discuss some thoughts toward WAD diagnosis, its’ unique attributes and potential rehab strategies.

A MUCH NOVEL STIMULUS:

The first factor of whiplash to mention might be its uniqueness: it’s the opposite of an insidious onset, and puts the body (the cervical spine in particular) through a particular load at a particular speed that it is likely very unfamiliar with. Taking all other factors out of the injury (the emotional trauma of being hit by another vehicle) this rapid change in tissue homeostasis and change in mechanical load and tensile forces detected as afferent input is impossible for the brain to ignore. There are all sorts of tissues being stressed: facet, ligaments, soft tissues and all their inherent sensory innervation. Mechanoreceptors responsible for communicating muscle tendon tensile status to the brain, are registering something off the charts.

Why is this situation, the sensory innervation being bombarded with new information, particularly conducive to a pain state? Part of the answer is context, part is that this how our bodies are designed to respond.

TRIGGERED RESPONSE:

When our tissues undergo abnormal stresses and strains, regardless of insult to tissue integrity or physiological changes in the tissues from these forces, our body (via our brain) “lets us know” and becomes temporarily sensitized (after that is, ensuring that we are going to survive). This sensitization is especially in tune with not only the specific way the tissues were stressed, but also the environment they were stressed in. This is where the analogy of a sunburn can be of use: the day after a sunburn, what does being in the sun feel like? Is that sun any different than the day before? No, but it sure feels different. Its your bodies way of telling you it experienced more than average of some stimulus, and it is going to create a scenario where you can now monitor this, and be aware of this. Without going into the minute intricacies of sensitization, the basic concept is that the tissues that underwent the most stress are going to then register similar stresses with heightened awareness, and as potentially threatening. This will continue until the tissues return to normal homeostasis, or adapt to a new level of stress.

The evidence suggests that pain mechanisms can move or shift as time goes on and the relevance of the tissue lesion diminishes in an inversely proportional way to the relevance of chances in the central nervous system” – Louis Gifford, on WAD (7)

THE CONTEXT:

This is particularly relevant to WAD. You can have a “Triggered Response” that is highly variable depending on the context of that response. The reason patients seeking medical attention for WAD is ubiquitous and often difficult to treat is the context of the injury. Whiplash is accompanied by an inherently threatening situation (unlike most insidious pains) and often this situation can be blamed on someone else. Now you have a situation where the normal responses of pain, tightness, headache etc are under constant interpretation of blame: “If it weren’t for that (insert your profanity here)  I wouldn’t be feeling like this, look at all the difficulties I’m having with even mundane activity- all of this is because of that accident and that idiot driver”. All the symptoms are real, and initially true tissue damage is often present, but propagated by this reaction. If it seems hard to grasp that concept, think of how our current state of thought reflects in what we feel in our bodies. When we are stressed, anxious, depressed, it is easy to notice some changes in how our body feels. Especially that whiplash is often sustained by an increase in tone, thinking recurrent thoughts of frustration and blame just ramp up the current condition.

This brings to mind an experience I had a month ago with some late season snowboarding. I was slammed pretty hard after a failed attempt at a spin of a small feature, landing 90 degrees shy of where I wanted and catching a backside edge: which is always followed by sort of a body slam to the back motion and the head follows.

 
Shot from the GoPro at Keystone...

Shot from the GoPro at Keystone...

 

I rode the rest of the day, without too much worry to it. The next morning my neck had about 50% of its normal range, super sore, super sensitive. I couldn’t lift my head directly from a pillow for about a week- I needed to assist a little with my hand and then I was good. I kept busy at work and tried not to think on it much. I was more amused by it than anything: I knew it would go away, I’d had this before, and I could almost approach it with a sense of curiosity instead of impending doom. This could be a key factor in a normal recovery and good outcome.  I realize my mini-whiplash was probably much less intense than many WAD patient incur, but there are some useful principals in management there. I am sure, that if the exact same stresses had have occurred, but as result of some car not paying attention to what they were doing and slamming my car, I my pain would have responded differently. I might be better and trying to meta-cognate on the influences of pain, but I wouldn’t be surprised if the recovery was 2-3x longer, and accompanied resentment toward the driver (why do I have to work all day with stiffness and pain because you weren’t paying attention??). Instead, I took complete onus for the event, thus I was really just waiting for tissues to undergo their proper physiological process after the high stress event, and viewed the symptoms as expected temporary changes.

I’ve actually tried a tactic (verdicts still out whether its appropriate) with WAD patients, at the appropriate time (emotions subside and they are showing signs of grasping the situation and confidence) instructing them to “if you are willing, really try to reinterpret your pain for the next 4 weeks and act as if the pain you have now was from a fall you had last time you went skiing (or whatever activity they are into- maybe head-banging at a concert) If the idea seems silly then we will find lots of other ways to help get over this..”. The downside is appearing insensitive, but I think if you could reinterpret the pain and separate it from incident, this would help.

THE IMPLICATIONS:

The fact that the same “injury” or stress can fall upon tissue and that tissue react in vastly different ways is evidence that we are not after a specific tissue impairment here with these WAD patients. Moreover, we are seeking to be a catalyst in returning tissue to its normal state (unless there is reason to suspect true tissue failure, such as transverse ligament of the atlas rupture or odontoid fracture).  Even if there were “findings” of (enter manual assessment here) these findings are a response to injury, and a reflection of the CNS sensitivity. Applying techniques to reverse these are usually futile in a sensitive state: poking the bear can have its place in terms of looking for adaptations and desensitization, but with this cohort any poking needs to come from an internal locust of control buy having the patient work on being able to test their own limits with constant monitor of their response (this could be through simple exercise), as they have all ready had enough “outside influenced stimulus” as evident in their MOI.

THE DAMAGE

We must first note the often tenuous link between what we view as “damage” and whether or not that is influencing the pain. We just don’t have a clear view of this. Some of it may be from lack of sensitivity of imaging, and much is from lack of true relation. However, damage aside, inflammatory responses can be viewed as somewhat causative. It may be better to look at tissues response (whether muscle, ligament, disc or facet) rather than its actual state (facet arthropathy, annular tear, disc bulge).

 
 

There is surely potential for damaged tissue post the stresses induced by whiplash. However, seeking to locate the damaged tissue and affect it manually by simply applying inputs may prove futile. Tissues heal at vary different rates due to their blood supply (so disc and ligament may be delivering their inputs to the brain for a long time post injury, thus creating a scenario more conducive to pain, with prolonged chemical or metabolic activity happening at the site of the lesion) and it is further difficult to pinpoint specific tissues with specific tests. Further, think about the relation between tissue abnormalities and pain- it is certainly not always a clear link.

While evidence from in vitro studies indicates that the injury can damage any number of anatomical structures in the cervical spine at any segmental level, it is largely unknown if these lesions occur either in combination or are independent of one another. However, one thing remains clear: whiplash injury can, in some patients, trigger a cascade of events that promotes the development of chronic symptoms. It is, therefore, crucial that emphasis be directed towards understanding the underlying mechanisms and subsequent sequelae of the condition” -Jim Elliot (1)

THE REHAB

We can’t think along the lines of “fixing the (facet, disc, or muscle)” or have the patient be under the impression that this is the absolute pathway to recovery. We also can’t think along the lines of “just let it heal” either, because the seemingly culprit lesion may only be relevant in initial stages of trauma, and the chronicity of pain driven by maladaptive changes in processing. And there isn’t one access point to these maladaptive changes: its multi-factorial. This means striving to consider how the patient thinks about their condition, their beliefs of injury, their additional stressors (litigation, job stress, road anxiety), their movement habits (the list goes on) have impact on the current disability, and how these areas might me modified or re-conceptualized.

"Emerging evidence suggests that clinical focus should be directed towards treatment schemas that better address identified dysfunction and clinical examination findings that have been shown to characterize the acute and chronic conditions (eg, alterations in the sensory and motor systems, and signs and symptoms of psychological distress)." -Elliot (1)

All pains are multi-dimensional, and “biopsychosocial”, however WAD pain is an especially “3D” pain due to its context:

Sensory Dimension: (afferent inputs, perception of pain and where it is, its’ behaviors and “attitudes”) *where most practitioners focus

Cognitive Dimension: How we process what we are feeling, our beliefs, essentially how our thoughts affect our pain; “this person did this to me”, “I have a disc degeneration”, “my spine is messed up”...

Emotional Dimension: with pain come emotional reaction: how our behavior changes, how we approach our environment in reflection of our pain.

"Pain is a biopsychosocial experience that goes well beyond mere nociception. In this regard, identification of the physical pathology at the site of injury is necessary but not sufficient to explicate the complex process by which somatosensory information is transformed into the physiological, cognitive, affective, and behavioral response labeled as pain" - Garland (2)

 What is a WAD patient working with?

  • High stress and anxiety, usually a "sympathetic dominated state"
  • Possibly centrally mediated somatosensory alteration (1)
  • Widespread sensory hypersensitivity (or decreased pain thresholds) (1)
  • Presence of muscular degeneration (fatty infiltration) in the cervical extensor muscles (1)
  • Dizziness and disturbances to the postural control system (5)
  • Impaired neuromotor control, detected in the CCFT (crainio-cervical flexion test) (4)
  • Reduced standing balance and increased sway (1)
  • Reduced cervical ROM (especially in rotation) (6)
  • Possible oculomotor dysfunction (3)
  • Jerky movement, not your normal smooth motions (altered motor strategy and co-contraction)

There is no recipe or protocol for WAD patients. We can apply what we know about sensitivity, how tissue reacts, concepts of graded exposure and relaxation, and patient assurance in seeking a good outcome.

I think the initial visit needs to be met with highlighting some of the above commentary: there is no “quick fix” but this doesn’t entail that something is broken. Tissue damage can definitely exist in the acute stage, but the patient should be taught to view their tissues as de-conditioned as opposed to damaged. This will allow them to have more confidence in their rehab. They also need to tune in to emotional influence. It is often pretty transparent to the patient that their emotional response is affecting their pain: they often claim that driving is very difficult and accompanied by lots of pain, stress and tension. I have had a few patients that I have instructed to just go sit in their car for 10 minutes, a few times per day (these were the patients that would break down to tears when even talking of the incident, and refused to get behind the wheel). This is an example of graded exposure: first sitting in the car, then driving around the block, then ramping up from there. These tactics are not directly aimed at the tissue obviously, but indirectly affect the tissue through how the body responds to situations, with the hope of less response over time.

To assist in reducing tone and prompting a more "parasympathetic" state, diaphragm breathing is always taught with this cohort. The relationship between sensitized state and sympathetic nervous system activity, and its counterparts can be explained if desired.

As with any rehab program, movement and strength are going to be important, and trying to find the balance in how much you can push these elements will be based on patient response.

·      High sensitization: patient education, belly breathing, very light self assisted cervical isometrics, small ROM exercises based on trying to “relax and move” such as fluid figure 8 movements in a small range and progressing from there, working on “indirect rotation and movements” from the bottom up, walking and introducing exercise distal to the sensitive tissue (cycle etc). Educate on the fact that their tissue response is normal, and that not moving or rest is actually more detrimental. Exercise may be used distally (like cycling) for  psychological  benefits as well as vascular benefit. The risk of manual therapy does not out-weight the benefit in this group.

·      Low sensitization: same as above but working on increasing intensity as tolerance allows. Deep neck flexor exercises, prolonged isometrics, upper body exercise,  and hopefully a program of return to activity they enjoy that is graded in intensity.

The “strength” exercise may be supplemented with education that “were trying to get the muscles to start acting normal again and responding how they should to work (not explained as your core neck muscles are very weak and can’t support your head). Patients may have overactive superficial muscles and weaker deep muscles as Jull notes with the CCFT performance in a WAD cohort.

 
The Cranio-Cervical Flexion Tests: Jull et al. 

The Cranio-Cervical Flexion Tests: Jull et al. 

 

As noted, muscle tissue makeup also undergoes changes. These areas which gain fat infiltration are known for their proprioceptive density, which could explain some of the loss of motor control and balance that accompanies WAD. This finding was also specific to WAD population (and not in chronic neck pain population) thus it is likely not only from disuse. Inflammatory processes may be more culprit in this finding in WAD patients, and WAD patients also differ in sensory and psychological measures (what I interpret to mean is that WAD patients tend have an overall more central sensitized state and remain so…)

Decreased range of motion may reflect underlying disturbances in motor function as a consequence of the initial peripheral nociceptive input resulting from injured anatomical cervical structures. (1)

The muscles are inhibited or using abnormal strategy, and sensitive to work because it is a form of stress. It is safe stress, but the body doesn’t always decipher that, so we can always find a starting point and slowly build up. Prolonged bed rest is only going to push back this starting point, as we need these tissues to be experiencing things, and we expect this to initially be a bit difficult and sore.

We need to also contemplate whether/how much the patients beliefs and attitudes are holding them in a state of altered motor-control, increased stress, tissue hypoxia, and overall maladaptive way. 

“Recent evidence suggests that disturbances to the postural control system are more likely to underlie these symptoms due to traumatic damage to the vestibular receptors, neck receptors, or directly to the central nervous system. Dizziness of cervical origin has been defined as a non-specific sensation of altered orientation in space and dysequilibrium. It originates from abnormal afferent activity from the extensive neck muscle and joint proprioceptors, which converges in the central nervous system with vestibular and visual signals, confusing the postural control system”  -Treleaven (5)

WAD patients demonstrate altered “Joint Positional Awareness”, meaning that they are not as good at telling where their head is in space. The research noting fatty infiltration in some of the proprioceptive dense tissues in the suboccipitals, which could account for some of this deficit, as well as general balance and motor control deficit. You can both assess and train positional awareness with a simple laser pointer and target. You can also work on motor skill, by slowly tracking patterns on the wall with a laser, at various speeds clockwise and counter clockwise. WAD Patients also have larger loss of ROM, particularly in rotation (possibly due to hypertonic or unwilling AA rotation via suboccipital tone?) though efforts to re-gain this in a non-threatening way and re-train this with motor control may be of value.

As we have seen in other areas of the body, even after patients become pain free, they still show deficits in positional awareness and muscle endurance, which could (possibly) set a stage for recurring injury. Below are some examples of exercise, that can be an adjunct to your typical program of graded exposure towards ROM and strength and addressing cognitive and emotional influences of pain. 

SOME EXAMPLES OF EXERCISES USING VISUAL FEEDBACK:

Below are some examples of potential exercises:  you could also do without visual feedback (the visual feedback just allows an external focus and makes motor control and strategy visible to both patient and practitioner. I find it sometimes helpful to use because it directs attention away from neck movement per say, and more towards the goal of making the laser move, which is accompanied by neck movement). "Indirect rotation" techniques allow the tissues to undergo stresses into new ranges in a different context (perhaps less threatening) and can allow the patient to realize the can move (show them after the exercise, "see you just rotated your neck fully with very little pain")- this might be encouraging. The "motor control" components are attempted to re-establish fine motor skill with constant scrutiny to accuracy from the visual feedback. This can be applied in various positions (neutral standing, seated, in rotation standing, or seated, standing on one leg, combine with a verbal or other body task etc...). Further, simple balance exercise may be warranted to allow the patient to practice postural control mechanisms globally. 

SET REALISTIC EXPECTATIONS

Explain that abolishment of pain after WAD is typically slow, for reasons mentioned above. Explain that it is very common to have a roller coaster like pain, where one day it will flare up for no reason. Explain flare-ups as protective behavior, and the body acclimating to the demands of life again. If there is rapid progress, great! If it is slow, than that is normal. We can’t force a tissue state to change and need to respect that, but we can attempt to effect all things influencing it.

-Tal Blair, DPT

 


REFERENCES:

1. Elliot et al. Characterization of Acute and Chronic Whiplash-Associated Disorders. 312 | may 2009 | volume 39 | number 5 | journal of orthopaedic & sports physical therapy

2. Garland. Pain Processing in the Human Nervous System: A Selective Review of Nociceptive and Biobehavioral Pathways. Prim Care. 2012 September ; 39(3): 561–571. doi:10.1016/j.pop.2012.06.013.

3. Heikkilti et al, Cervicocephalic Kinesthetic Sensibility, Active Range of Cervical Motion, and Oculomotor Function in Patients With Whiplash Injury . Arch Phys Med Rehab Vol 79, Sep, 1998

4. Jull et al. CLINICAL ASSESSMENT OF THE DEEP CERVICAL FLEXOR MUSCLES: THE CRANIOCERVICAL FLEXION TEST Journal of Manipulative and Physiological Therapeutics Jull et al 527, Volume 31, Number 7

5. Treleaven, et al. Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. J Rehabil Med. 2003 Jan: 35(1):36-43

6. Woodhouse et al. Altered motor control patterns in whiplash and chronic neck pain BMC Musculoskeletal Disorders 2008, 9:90

7. Gifford. Topical Issues in Pain 1. Whiplash: science and management Fear-avoidance Beliefs and Behaviour. AuthorHouse Publishing. 8/30/13.

Fluid Motion: how multiple aspects of pain experience can inhibit our free flow

Tension is who you think you should be. Relaxation is who you are
— Chinese Proverb
fluidROM.jpeg
Motor responses reflect the CNS response to pain , threat, emotion, pathology, lifestyle, environment and task demand
— Peter O’sullivan

Normal movement is easy, and focus is away from the body (external focus). People in pain have an internal focus, and move in a less fluid sense. A perfect example of this is what is known in baseball and golf as “the yips”. The term was coined by the Scottish golfer Tommy Armour, who said it was a "brain spasm that impairs the short game."

 
#fail

#fail

 
We act in accordance with our self-image. This self-image-which, in turn, governs our every act-is conditioned in varying degree by three factors: heritage, education, and self-education
— Moshe Feldenkrais

 

The concept of psychosocial factors influencing our movement has been present in some form of therapy for a long time, as noted in this insightful Feldenkrais quote (an opening line in his "awareness through Movement" text circa 1972). How your patient thinks about their condition, about how fragile they are, about social ideas and common beliefs about pain, can all impact how a they goes about in their daily life from how they get out of a chair to if they participate in light exercise. 

People with chronic low back pain move with less lumbar ROM and show proprioceptive deficits, in comparison to people without pain (as noted in Laird et al's systemic review and meta-analysis)

The fact is, when we’re in pain, we consciously think more about our body. We have constant reminders to do so. Our experiences along with our conceptions work our way into our psychology and can become a cyclical pattern, often self propagating after injury. The Physical Therapist has to help decide whether the motor responses and movement strategies are adaptive (protecting the physiological components of the body to avoid further injury or inflammation) or maladaptive (the motor responses are actually adding to the problem). 

 
 

I was fortunate enough to attend a cognitive functional therapy workshop with Peter O'sullivan, and it was a fantastic course discussing how people's beliefs can change how they move and interact with their world.  Can people actually adopt a pattern of moving that makes them worse? Yes… the question is WHY? And this is where we need to address psychosocial issues, and in my opinion possibly relate them to tangible biomechanical (and easily understandable) concepts when appropriate. Are restraints to movements physical, psychological or both? The fact is, teaching people to move “differently” can help them, for the sole purpose of creating an atmosphere that breaks the Load-Pain-Thoughts relationship, to place a schism in the circuitry that is currently set to manifest as a painful experience.

Tactics in changing movement and load habits can really vary, and be a common variable in positive outcomes across many different philosophies of treatment, despite the specific intention of the intervention. Examples could vary from something as simple as moving a computer monitor from the left to right side of the desk, considering if and when you exercise, or deconstructing movement during a task to inhibit some of the altered adaptations brought on by the initial injury or perceived threat.

One side-note that is important to address however is that this isn’t and eternal tactic of pain relief; meaning that we should be able to sit erect, or slouched, or whatever (really without thinking on it) and it is natural. Once we have successfully calmed down the adverse response, our goal should be to return to all movements available (in my opinion even if these are again temporarily associated with small amounts of pain, because we don’t want underlying fearful thoughts or subconscious pain neuro-tags to continue to reign dominance over a persons behaviors).  People are supposed to move again. Even persons with multi level lumbar fusions play golf and return to unrestrained movement (this should be encouraging for your spine patients to hear).

Is pain itself, and the consequences of living in a current state and experiencing a past state of pain, up-driving physical adaptations (increased muscle activity) leading to a cycle of pain experience and behavior?

Subgrouping the patient with pain can help addressing loading habits: is there a loading strategy that exacerbates pain?

·      Is the patient holding themselves in extension and having excessive muscle activity and avoiding flexion

·      Is the patient holding themselves in flexion and avoiding extension?

Communication can be difficult, even in moderately acute cases of LBP, but especially in chronic cases. Consider relating to an ankle sprain: what would happen if you did injure your ankle? Swelling, stiffness, hypersensitivity and pain right? What do you think would happen to the ankle if a year after the terrible sprain, you were still limping, guarding, and avoiding moving it? In general, what do you think would help the ankle get better?

*but what if the tissue is damaged?

Things can get damaged: cartilage can become malnourished, and chip off of its underlying structure. Surrounding muscles can undergo physical and chemical changes, and become significantly less robust.  Regarding LBP, some of the most emphasized tissue-issues we hear about in life is facet cartilage (facet arthropathy) and disc degeneration. (you could explain the damage and pain relationship here, I often bring up that complaints of LBP doesn’t correlate with age, though age and radiographic degeneration have a linear relationship…it is not a fact that all grandparents must have spine pain….)

What is also important to realize however is that:

·      Even if there is physical damage, such as a osteochondral lesion or cyst, highlight the message that the effects of prolonged immobilization are further deleterious to the actual tissue. The best bet effort in moving forward with life is to move and strengthen in some capacity. Go back to the ankle example: knowing that joints need movement to nourish cartilage (synovial fluid production), what would happen to this environment after injury if movement ceased?

·      There are times when tissue morphology and tolerance to load result in constant inflammation and constant poor environment to the tissues. In these cases an attempt in adaptive changes to minimize load based on morphology of the structures (think cam-pincer of the hip) are to be implanted while maximizing movement and strength in the ranges that are not threatening. Seek to further gain use of motion above and below. Surgery can be an option, but is usually a last resort. Even when it is on the table, conservative measures still needed to be exhausted,  and persons educated on what this entails and why, to deconstruct the thinking that once the “wear/tear” is present that it equates eternal pain.

Do the biomechanics matter? Yes, because these are one thing (among others) that we can modify in some Macro-capacity: I say “macro” because research notes that efforts on specific manual technique to attempt to address specific joint biomechanics is misleading. When we think of what we can truly impact, we are talking adapting positions, habits, and how our body acts in positions, to change biomechanical inputs. We may attempt address them in a specific “Micro-capacity”, but need to understand the mechanism is not well understood nor specific to the majority of the intentions of MT “techniques”.  These may be acting under DNIC “diffuse noxious inhibitory control”, placebo via explanation and delivery, or novel experience guiding the patient into new movements and sensations, and the patient allowing their tissue to alter its response under the context of a therapeutic intervention. However it is much more likely that we are addressing underlying tone and the CNS response to the perceived threat, than addressing specific joint or tissue mobility as a culprit to the behavior and movement adaptations.


A pain flare up can be a biomechanical trigger on a sensitized system.
— Peter O'sullivan

The conundrum for PT and patient alike is evident in any pain labeled “chronic”: my “healing” isn’t happening. Perhaps it is slow because the insult was to avascular tissue, the insult is recurrently agitated by underlying sensitivity to load and overactive inflammatory processes, or there is no actual insult at all albeit the tissue at a local and global level is responding as such under maladaptive CNS changes, and altering what should be a normal environment and inhibiting resolution of what was acutely considered adaptive and normal. There is not a perfect explanation, or treatment for these conditions, but finding a pathway to changing mobility and loads, strength, and patient perception are things to strive for.

Some useful examples in promoting new or more fluid motion:

·      “the clenched fist”: Clenching a fist isn't painful, but it might be if we were always doing it... see the white knuckles? these tissues aren't getting nice blood flow, and the tissues are under increased load and stress.

 

 

·      “the Yips” analogy: over-concentrating on movement can lead to decreased performance and lack of fluid effortless motion.

 

·      “Immobilization leads to tissue breakdown” analogy: NOT moving isn't a healthy option, unless the tissue is truly needing to repair its leisiion (fracture or ligament tear)

 

 

·      Parasympathetic diaphragm breathing in relation to sympathetic pain response: explaining how our present state can affect pain and response, and ways to calm this.

 
 
  • "Some form of movement and loading is almost always safe": It may be helpful to ask a patient what the first thing a person with a total hip or total knee does after surgery (they walk and load the tissues). This illustrates that even in situations where prosthetic devices are drilled into bone, doctors allow patients to walk because the loading is necessary for healing and good outcomes. 

One way to break into changing movement or introducing novel movements (accessing change through movement and exercise) can be to work on dissociation of movement. This concept is fairly simple, and its mechanism of effect could be argued though likely contributions are novel movement experience, body awareness, and physiological benefits of moving through ROM (perhaps in a way that conflicts with maladaptive movement caused by muscle tension and protective behavior).

Further you can use an additional "external cues" to break cycles of internally focused movement and add engaging novel exercise while allowing the patient to see how effortful or effortless they are able to move at will, and how much motion they have in one direction compared to the other.

See a few video examples below:


 

 

-Tal Blair, DPT

What is my Inferior Temporal Gyrus? And why haven’t I up-trained this mother for my ACL Clients?

ACL injury is prevalent in athletics.  Not only are there immediate injury and changes, but there is substantial evidence that there are long term changes associated with this injury including: osteoarthritis, alterations in gait, changes in body awareness and psychology, and weakness as well as increased risk of further musculoskeletal injury compared to non-injured individuals. Even more studies have reported unresolved neuroplastic changes after injury, reconstruction, and rehabilitation that may limit function and return to sports participation.  There has been a large focus in the past decade of creating preventative programs and limiting exposures to potential injuries through conditioning and body awareness.  However, decreased body awareness is inevitable with ACL injury.  Trauma to the ACL has been shown to modify how the nervous system processes the interactions between vision and sematosensation. The loss of previously recognized reflexes and gama motor neuron drive to prepare the CNS function to engage appropriately may require “up-training” of other systems, such as increased utilization of visual feedback, to maintain the required sensory input for motor control.

Recently in JOPST, Dustin Groomes, MEd, ATC, CSCS, from The Ohio State University recently discussed the importance of understanding the changes in body systems and neuroplasticity after ACL injury.  Groomes describes how training the biomechanical factors of the ACL injury may not address all the physiologic consequences. But the capacity for neuroplasticity after injury and during rehabilitation can present an opportunity to close the gap by targeting a broader spectrum of sensorimotor function during neuromuscular training.  This can be captured by the non-contact (majority) ACL injury.  Generalizing the break down of the typical action is:

  • a failure to maintain knee neuromuscular control while attending to an external focus of attention under highly complex visual stimuli, variable surfaces, movement planning, decision making, during classically an open environment. 

During this changing environment, the sensory systems 3 main afferent pathways of vestibular, visual, and somatosensory provide complex integrated information.  This is rapidly acquired and processed to produce efferent neuromuscular control to maintain adequate stability and control.  The interaction between vision and somatosensation is particularly critical for motor control during environmental interaction. This interaction is compromised even after ACL reconstruction. The ACL receives nerve fibers from the posterior articular branches of the tibial nerve. These fibers penetrate the posterior joint capsule and run along with the synovial and periligamentous vessels surrounding the ligament to reach as far anterior to the infrapatellar fat pad. Disruptions in this input yield immediate changes in neuroplasticity and can lead to mechanical changes and compensations that may not be properly or fully rehabilitated during typical training focused solely on biomechanical changes and strength gains.

The loss of ability to relay on the bodies typical reflex afferent inputs may require “up-training” of supplementary mechanisms such as increased utilization of visual feedback to train and maintain required sensory inputs for motor control. 

Groomes further states that individuals in his fMRI studies demonstrated increased activity in the posterior inferior temporal gyrus.  This area has been linked to many cerebral functions, but may primarily be involved with visual processing of movement.  This area must work together with the hippocampus, in order to create an array of understanding of the physical world. The information received in this area is sent to the Primary Visual Cortex (V 1) for processing determining the outputs from the Motor Cortex (M 1). The increased activity in this area post ACL injury may suggest that there is an increased utilization of visual processing and motor planning for movement simultaneous with depression of the somatosensory function of the ACL previously discussed.

Simply put, the body is nothing except adaptable.  Even in ways that we don’t even understand, yet.  But it seems that if we injure our ACL, the brain automatically changes its preference to more visual based inputs to assist in making decisions for motor control.  What about those who aren’t injured yet?  On the flip side of that coin, Swanik reported, in 2007, initial findings of decreased visual reaction times and processing speeds as predictive of ACL injury. Perhaps we need more visual based processing and challenges during our preventative strategies as well?

This begs the question.  What are we doing for enhancing visual feedback for our ACL or currently healthy clients? How are we up-training them visually in the attempt to prevent overload in the athletic environment?  If we know they can’t feel the knee like they used to….literally…how can we impose a greater demand on vision to help adapt more than there body, but also their brain?

Here are a few tips on how you can start addressing this need with your clients:

1)    Start changing our cues and attention to an External Focus (see our blog on external focus) (Links to our external focus webinar)

2)    Ensure that we are challenging our clients in an open environment, as soon as it is safely possible, performing dual tasks frequently

3)    Consider giving you and the client immediate visual feedback during skill training early in rehabilitation with a device such as the Motion Guidance Clinician Kit

4)    Consider taking visual feedback away at times during advanced mechanoreceptor training exercises to continue to challenge the body with different inputs.  This might be particularly challenging for the client on altered surfaces or to advance already mastered skills

 

Hopefully this information has stimulated your own approach to rehabilitation of this challenging population.  We need to be aware of utilizing all possible body systems to maximize the ability of our clients to be ready to return to their best potential in their athletic or work environments.

 

-Eric and Tal

Motion Guidance

Performance Strategies: Striving for the "Triple Play"

For those who have followed this blog, one of the most researched backed uses of the Motion Guidance Clinician Kit is providing an External Focus (EF) of attention during movement.  Combining EF with immediate visual feedback can provide accelerated learning of motor skills acquisition and performance for any user.  But recently, I was at the Combined Sections Meeting of the APTA in San Antonio, USA and had the privilege to listen to a talk by Gabrielle Wulf (University of Las Vegas, NV) on the recent advances in Motor Learning.

Gabby Wulf (if she’ll pardon the casual reference, but she was introduced as such at CSM) is one of the front leaders in motor learning and performance research in the past 25 years.  She has been the lead author of both books and professional journal publications.  Gabby spoke on new developments in Motor Performance and retention and what she was referring to as the “Triple Play”.  This blog will give an overview of her publication and the concepts behind this Triple Play for Motor Learning and performance.

HOW YOU CAN IMPROVE YOUR CLINICAL INTERACTIONS BY ADDING “TRIPLE PLAY” CONCEPTS

First, there needs to be an understanding of what the definition of motor performance is for this blog, which I will define as “the ability to learn and retain a motor skill in a controlled environment over several trial and repeated sessions.”

Now lets talk about three separate motor learning strategies, discussed in the study by Gabriel Wulf:

  • Enhanced Expectations
  • Autonomy Support
  •  External Focus of Attention. 

I will break these down into each individual section and then come back around to the results of the study.

Enhanced Expectations

This concept refers to the description of augmented social-comparative feedback in a positive form. It is essentially not setting definition on success, and allowing the person to define success through performance.

Lets use an example of  Enhanced Expectations with an archer and target:

A typical target is made up of colored circles in which the smallest circle and color might represent the “best” attempt.  The participant might automatically assume that certain colored rings are more successful than others.  If we consider this example of the multi-colored target.

One way of implementing Enhanced Expectations to shooting at this target would be to give feedback that ALL attempts are successful if they simply hit the target (or using a target with all one color). This lets the archer then decide for themselves what their success means as they become more accurate, and their motivation is based on their experience as they dictate how accurate they want to become and challenge themselves.

Autonomy Support:

I hold this massive key, what will I choose? 

I hold this massive key, what will I choose? 

This concept gives the learning a choice in how they can complete the tasks, allowing the person to be autonomous and lean based on their choices.

In the archery example, the archer could be given the option of holding their arrows in their quiver or being placed on the ground or rack.  If you wanted them to shoot a total of 30 arrows, you could allow them to choose how many arrows they want to release in each block trail (instead of 3 sets of 10)

External Focus of Attention:

This concept has been well documented in numerous studies as showing superior learning and retention for motor learning compared to Internal Focus. It is essentially directing attention externally during the task.

Changing our thoughts and our words to describe the goals of the movement rather than the body actions that are required to complete the task can be difficult for the practitioner, and may take some creativity, but doing so allows optimal learning.   Being aware of how we give cues and feedback can be critical to performance.


THE RESEARCH:

The design of this study included 4 groups with various feedback styles implemented (click the slide to the right to link):

  • Enhanced Expectations - Autonomy Support (EE-AS)
  • Enhanced Expectations - External Focus (EE-EF)
  • Autonomy Support - External Focus (AS-EF)
  • Autonomy Support - Enhanced Expectations - External Focus (AS-EE-EF)
A slide from Gabrielle Wulf's presentation at CSM 2017

A slide from Gabrielle Wulf's presentation at CSM 2017

Participants threw balls at a target with their non-dominant arm. In the Enhanced Expectations conditions, they received positive social-comparative feedback. In the Autonomy Support conditions, they were allowed to throw with their dominant arm on trial blocks chosen by them. In the External Focus conditions, participants were asked to focus on the target. On a delayed retention test, the AS-EE-EF group outperformed all other groups (click on photo for your hyperlink to the article abstract).

The findings provide evidence that enhanced expectancies, autonomy support, and an external focus can  all be combine to optimize motor learning.                                 

These results should give us further awareness into how we can maximize the learning, performance and retention for our patients. 

LETS USE THESE FEEDBACK CONCEPTS IN A CLINICAL EXAMPLE:

Mr. Jones is 3 weeks after his Total Knee surgery. He is struggling with quad lad during SLR, poor quad set initiation, and lacking 8 degrees of active extension.

Enhanced Expectations: 

Mr. Jones is laying supine on the plinth working on extension:

  • Option A) "I want you to straighten your knee, we want your knee totally flat on the plinth. Squeeze your quad muscle and try to get the back of the knee flat and hold for 3 seconds".

  •  Option B) (small towel placed under knee laying supine) "If you feel pressure on this towel, you are successful in this exercise. Practice this for 3 seconds on, 5 seconds off, over the next few minutes".

 Option B uses Enhanced Expectations : Mr. Jones gets to advance himself based on what he is feeling and how he is performing.

 Autonomy Support

Mr. Jones is now moving on to doing some walking, he is using his walker.

  • Option A) "I want you to walk for 5 minutes, going back and fourth from the wall with the therabands hanging on it to the door over there, holding your walker close to you with a light grip on the handles…"
  •  Option B) "Were going to do some walking, and you get to choose the distance, I will be timing us. We will do a few bouts of this. You can go where you like, down the hall, or stay in the clinic. Hold your walker how you feel most secure, though as you advanced you should depend on it less and its easier to walk erect if the walker is closer to you".

Option B uses Autonomy Support: Mr. Jones gets to choose how he performs the exercise, and he can modify this based on his experience. His performance isn’t pre-determined or strictly defined, he is in control of this.

 External Focus of Attention:

Mr. Jones returns for the next session, and he thinks his leg is getting straighter but not sure.

  • Option A) "Mr Jones, you really need to be squeezing your quad muscle with this. Lock it out. Squeeze that quad and straighten your leg".
  • Option B) "Mr. Jones I want you to watch your knee cap and try to elevate it. Your goal is to see some wrinkles above the knee cap, then hold these wrinkles for 3 seconds".

 *Alternatively, if you have a visual feedback set up, the external feedback addition is pretty simple: “Mr. Jones I want you to make this laser light go further down your sock every time you attempt to straighten the leg”.

 

Option B uses External Feedback: Mr. Jones isn’t trying to internally and cognitively think of his body and what its doing, he is able to focus on something else out side of the body, that is directly related to the task in a way that allows him to judge visible success.


Another simple example of applying these concepts with the  Motion Guidance device  is during an exercise such as the “bird-dog”. I have started to change how I instruct patients during this simple exercise in clinic.

 
 

Classically, I place the drop target (black and white bull’s-eye) under the patient with the laser turned on. I have now started to not give a pre-determined goal to the patient during the exercise.  But rather, I use Enhanced Expectations to give delayed feedback that keeping the laser on any part of the target during the exercise was a very good result (instead of suggesting that the closer to the center of the target the laser remained was the goal). 

Not surprisingly, the patient independently wants to improve their precision during the task in subsequent blocks. Then, I give Autonomy Support by allowing the patient to determine how many repetitions they want to do on their first set.  Then I pay attention.  How is their performance?  What strategies is the patient using to get this performance?  The real beauty is that External Focus is already provided to the patient by the laser.  LET THE LEARNING AND RETENTION BEGIN!

Hopefully this blog has given you some extra considerations about the strategies we are using with our patients during motor skills training….and EVERYTHING is really some component of motor skill learning.

-Eric

Tactile Chicken Soup for the Brain: 2-pt discrimination

Reorganize, sharpen, and hone the body schema

This guy has nothing to do with that statement, but looks like someone who might say that...

This guy has nothing to do with that statement, but looks like someone who might say that...

Today’s blog will discuss some interesting research on cortico-somatosensory reorganization, and its implication to pain patients and the art of physical therapy as a whole

One factor that can feel unsettling is summarizing or justifying treatment with a much more complex explanation of mechanism,  in part due to patient education, though as practitioners  we just have to accept that humans are complex and continue to strive to find meaningful variables, explanations, and interactions that promote proper beliefs on behalf of the patient regarding their condition.

The practitioner may want do delve into a deep understanding of treatment interaction, mechanism of effect to interface (tissue being “treated”), application of treatment and education, all for the purpose of building a proper framework. From patient perspective however, I believe simple is better: we can choose to communicate concepts of the body recovering to its normal state (ie getting rid of pain or restoring function) to patients in a way that borders the conversation between two laboratory physiologists students prepping for an exam, to explanations that are tangible to the patient (though may seem trite).

This can be a particular area of struggle for myself when internalizing the way a patient presents, then externalizing it verbally in terms of approach to explanation of symptoms, treatment, patient buy-in, adding a bio component that is meaningful as well as psychosocial component that is tangible and meaningful. Beyond that, there can be many other intended influences passed upon the patient that don’t necessarily warrant an explanation (maximize placebo effect while setting realistic expectations and practice good listening and empathy skills with explanations that don’t dismiss or belittle patient concerns).

We do this all the time, decide what to verbalize and what not to; some of it is subconscious. We don’t start an evaluation by saying“research shows that good eye contact and listening when talking to people in pain during their initial sessions is predicative of a good outcome” then sit watching the patient and nod… but with all the information on a persons response to treatment elucidated by placebo studies, psychosocial studies, and pain science in general we have a lot to choose from in terms of what to and what not to verbalize.

Which brings me to the topic of a smudged homunculus…

 
 

 

I like to reference the studies by Moseley, as well as Louw, that discusses 2-point discrimination deficit in CLBP patients, when I find a reasonable time to do so with patients.

I think a meaningful way of getting some rather interesting and hopeful research across to a patient in pain may be something like this

When were experiencing pain, we start to move and act differently than before.  Initially this may be proper and important, as we want to protect the possible tissue injury, though if our body continues to react, move, and live as if injured it can become habituated.  We all have an internal map of our bodies in our brain,  and research shows that people with persistent pain start to recognize the part of the map representing the painful body part less. This results in improper interpretation of information getting to the brain, and affects what you feel as pain and how you move that area.

 A recent research study looked at sensation awareness in lower back pain patients, and they found that the people in pain had difficulty discerning how many pins were poking them, where they were and how far apart they were. The also found that they could train this over a few months, and the people had a significant reduction in pain once as they became better at noting the accuracy of the pin prick.

 Most interestingly, the people only improved if they were asked to scrutinize the sensations and report what they were feeling (placing pins into the back and creating a stimulus without having the patient consciously focus on what and how they were feeling it had no benefit).

 

 Although verbose, choosing to convey this info to the patient may be relevant for a few reasons:

·      It validates that in persistent pain patients something could be “wrong” or “amiss” for the patient, without describing damaged joints or tissues

·      It demonstrates that changes can be made, and points the periscope at the tip of the iceberg that there is more to getting better than “fixing the joint with a technique”

·      It shows the possible importance of awareness to the patient, that some portion of them improving will be pending on them making their exercises (or manual therapy) meaningful and not just “something done to their body”.

·      It opens up a window for more questions from the patient, if THEY want to learn more about it! (spouting intricacies of pain being an output may inhibit relations if poorly administered)

So back to practitioner framework, why is the research of impaired 2-point discrimination important? We know that somatosensory organization of the brain changes (maladaptive) when there is dysfunction (this is seen in not only pain, but post stroke). Loss of limb leads to invasion on the severed limb’s representation by surrounding area representations. It abides by the “use it or loose it” principle. That’s right, neuroplasticity can be for better or worse. Further, when we acquire a skill, these (adaptive) changes are reason for our performance and retention of that skill (why a professional violinist may have a differently organized map of the fingers). In the Motor cortex, neural density and cortical matter is correlated with the importance and use of that area!  It can be “sharpened” and adapt by training, just like it can be “dulled” by non-use and habituated pain behavior. The Motor cortex gets info/inputs from the somatosensory cortex and digests it in order to coordinate an output of motor control. Thus disturbances in output (how we move) are related to altered input from the somatosensory cortex. Though alleviating pain doesn’t necessarily mean the output of motor function, fluidity of movement, and movement options restore automatically. This is why functional movement based exercise is important, and in particular, perhaps awareness to movement. And the “functional” (although this term can be annoying) is important in that in order to be a catalyst towards a cortical reorganization change, it needs to be meaningful to the patient.

*as a side note, what annoys me with “everything must be functional” is that there needs to be a starting point with every patient; if their current function is maladaptive then replicating a functional exercise component may be difficult. Giving some form of input (maybe its an isometric, maybe just some simple pelvic rocking) may be a good starting point to build upon the awareness and ability, while educating the start slow and build concepts of graded exposure.

Although I know little of “Feldenkrais” physical therapy, I imagine part mechanisms of their success is due to this remapping that takes place, as they are “feeding” the brain with lots of slow and thoughtful inputs through movement. I still think an explanation is warranted on why the person should pay attention to the movement, as if not, the person is just knowing that “every 2 hours I need to do a pelvic clock, that’s supposed to make me better”…

I like how Tim Flynn and Emilio Puentedura discuss manual therapy in a recent publication discussing manual therapy and some of the paradigm shifts concerning “mechanism of treatment” (just because it “works” doesn't mean that the specific treatment was the “fix”)

·      “There is very little evidence that manual therapy performed under anesthesia is effective for CLBP and perhaps this is because we need to “manipulate”the brain, and not just the joints and other peripheral tissues, to bring about a change in the pain experience”…

·      Current evidence suggests that these representational body maps are dynamically maintained in the brain (neuroplasticity) and are negatively influenced by neglect, decreased movement, and pain

·      They touch on that part of skilled MT is certainly feeding inputs, as in “do you feel this part of your spinous process here, whats it feel like with this motion? Is this painful? Can you feel a slight stretch here?


These “techniques” can certainly be beneficial, but were continuing to consider lots of different reasons for their efficacy.  Physical therapists like Jason Silvernail have been talking about this for many years, in what he at one point titled “crossing the chasm” when speaking of some of the reconceptualization for what our treatment is doing. Finding ways to communicate these concepts isn’t always easy (with both patients and fellow PTs), but if you’re at all a curious PT its impossible to ignore.

Although the aforementioned study discusses sensory input via pin prick, the body is experiencing sensory input via movement all the time. The take home to me is that under the influence of altered inputs feeding a cycle of altered outputs, we are more hopeful of changing this if we add awareness and discrimination to our inputs: be it exercise our MT. Visual feedback may be one way being able to constantly re-scrutinize positional awareness, test and train. In this sense, we’re giving more information, which may change processing in hopes to achieve an overall more adaptive system.

MG.blog.pic.2ptouch.png

 

-Tal Blair, DPT

Share this blog on socials

Want to know when new blog content is uploaded? Sign up below:

!


References:

Moseley et al. Tactile discrimination, but not tactile stimulation alone, reduces chronic limb pain. Pain 137 (2008) 600–608

Catley et al. Is Tactile Acuity Altered in People With Chronic Pain? A Systematic Review and Meta-analysis. The Journal of Pain, Vol 15, No 10 (October), 2014: pp 985-1000

Louw A, Farrell K, Wettach L, Uhl J, Majkowski K, Wedling M 2015 Immediate effects of sensory discrimination for chronic low back pain: A case series. New Zealand Journal of Physiotherapy 43(2): 58–63.

Flynn et al. Combining manual therapy with pain neuroscience education in the treatment of chronic low back pain: A narrative review. Physiotherapy Theory and Practice · June 2016

 

 

 

 

 

Lunge Positional Changes and Altered Patellofemoral Stresses

The forward lunge is a common exercise in both home fitness routines as well as with personal trainers and physical therapist to increase the load and capacity of the lower extremity during resistive training.  While the forward lunge is very common, the biomechanics of how it is performed can vary greatly.  These changes may affect how much joint stress the kneecap undergoes. Recently in the Journal of Orthopedic and Sports Therapy, a research article (1) was published regarding these alterations and how they affect the stress on the knee.  The article addressed both the trunk and lower leg position and how they affect stresses at the knee during the forward lunge exercise. 

Cory et al investigated three varied, but similar positions of a forward lunge.  The three positions can be seen here.

 

What they found was the lead limb position influence both the lead and hind limb stress during the forward lunge.  With a forward trunk and forward lower limb positions, an increased stress was reported on the forward limb.  However, the stress on the hind limb as reduced compared to the FV and VV positions.  The opposite was found during the other trunk and limb positions during the lunge.  When the front leg was maintained as more vertical the force on the front knee limb was reduced, but at the expense of the rear limb which showed increased joint reaction forces during the FV and VV positions.

 
A recent published article in JOSPT in Jan 2017 reported altered PF stress during different types of shank and trunk positions during a lunge. Here are some visual feedback options using MG to standardize the performance mechanics for your patient.
 

These results can yield clinical considerations of varying the lower leg and trunk positions during the forward lunge exercise to either avoid or achieve a desired performance or reaction force at the knee joint.  Adding visual feedback to the trunk or the lower limb during the lunge may assist both the clinician and the client in achieving and maintaining the desired body position.

One option is placing the Motion Guidance visual feedback unit at the lower leg:

 
Laser positioned at knee.

Laser positioned at knee.

 

Another option to look at trunk lean and weight shift would be placing around the trunk:

 
Laser positioned at trunk

Laser positioned at trunk

 

can help provide and external focus to the biomechanics during the exercise giving an immediate visual cue to help performance and possible avoid long term “wear and tear” to the knees.

Eric

Motion Guidance.

share this blog on socials


Reference:

1. ) Hoffman, Cory et al. Trunk and Shank Position Influences Patellofemoral Joint Stress in the Lean and Trail Limbs During the Forward Lunge Exercise.  JOSPT VOl 47, No. pp 31-39, 1, Jan 201

Want to know when new blog content is uploaded? Sign up below!

Anterior Knee pain and the influence of the retro-patellar fat pad –Part II

We’ve just finished up discussing the anatomy and potential mechanisms of pain from the Retro-patellar Fat Pad of the knee.  This part II section of the blog is dedicated to clinical significance and treatment options.

Clinical Significance:

·       Distinct focus by the clinician to the quality of exercises like QS, SLR, and SAQ in open chained exercises will give valuable information about the possible amount of lateral displacement of the infra-patellar fat pad (IPFP), prompting possible mobilization of this area. Decreased efficiency of the quadriceps pulling on the patellar tendon or altered expectations of achieving full terminal extension during exercise may lead to decreased fat pad excursion and increased fibrosis or even scarring of the IPFP leading to Hoffa syndrome

·       Over the years, many patients have entered my care that report seeing previous PT, home skilled care, or have all ready been doing exercises given to them from the surgeon’s office or hospital.  “Oh I’ve been doing quad sets and straight leg raises at home”. After education and correction about the goal of the exercise, the patient often states “That is harder to do” or “That hurts doing it that way” or ‘That’s not what I have been doing at home”. Many have a good quad set that lacks ability to drop the knee into terminal extension, though demonstrate extensor lag during the typical flexion SLR.

Exam: This is where things might get difficulty as I am not aware of any objective testing specific to the IPFP (see Chad Cook publications for this possible info). My clinical exam typically involves passive extension to determine ROM at the knee, if there is the production of pain around the Anterior Interval (AI) and patellar tendon during this passive knee extension, palpation of this area for sensitivity (specifically to the lateral portion of the AI/patellar tendon), and quality of the patient’s Quad set and Straight Leg Raise.

If the clinician suspects anterior interval involvement then mobilization is warranted, and to be mixed with exercise. 

Treatment options:

·       Vigorous and/or prolonged manual mobilization of the anterior interval in multiple planes with graduated extension from 30-0 and even “passive-protective-hyperextension”.  This is where I love my Motion Guidance Manual Therapy Contact Pads.  There are superiorly sticky compared to other materials, with extra cushion to diminish contact soreness.  But most importantly, there are HYGEINIC! Washable after each use and they return to their original stickiness

 
 

·       Achieving full terminal extension ASAP. I would recommend this doesn’t mean “putting your body weight into it”.  Complimentary techniques such as Mobilization with Movement often yield wonderful immediate results and encourage the quadriceps to take over the new motion that is gained during the treatment session. And patient rapport will be likely maintained by not having just drilled them with a painful overpressure.

·       Loaded OKCE and CKCE with education on attaining full terminal extension during the exercises

 
 

·       And finally, as a last ditch effort, I have found prone knee flexion to be of great usefulness for IPFP mobilization.  Prone knee flexion draws tension over all structures at the anterior aspect of the knee.  Sustained low load, long duration holds can provide mobility to these tissues.  But WARNING…it hurts.  Typically I will put the patient in control of the intensity, as I can’t see their face in this position, to verbally tell me when they have reached a 7/10 (totally arbitrary on my part for achieving painful but tolerated tension) as a stopping point for the stretching.  To account for this type of painful knee , I will holster this type of treatment until around week 5-6 post-operatively for anything involving an anterior knee incision (ACL, TKA, Tib Tub Transfers, etc) or meniscal repairs). My reasoning?  That is the very early stage of the scar maturation phase.  Early healers will find this more as a stretch and appreciate the localized tissue mobility response.  Delayed healers typically have enough time post surgical to tolerate this aggressive natured mobility.

Hope this review and treatment options help you find extra success and happy clients in your clinics.

-Eric 

Motion Guidance

share this blog on socials

Anterior Knee pain and the influence of the retro-patellar fat pad –Part I

The front of my knee below my knee cap hurts!” How often do we hear that complaint in our clinics after injury, surgical procedure, or insidiously? 

One possible cause of this type of pain that may go undiagnosed is anterior interval impingement of the knee, a condition where compression of the infra-patellar fat pad (IPFP) results in pain.

In the typical healthy knee, the infra-patellar fat pad will displace posteriorly during knee flexion owing to pressure from the patellar tendon as the angle formed by the patellar tendon and anterior tibia decreases.  Conversely, extension moves the fat pad anteriorly away from the tibia.  Essentially in lay terms, the IPFP is sucked under the patellar tendon during flexion and is required to squish laterally and anteriorly around the patellar tendon to achieve full knee extension.

Teichtahl, in 2015, reported that a larger Cross Sectional Area of IPFP predicts reduced lateral tibial cartilage volume loss and development of knee pain and might act as a shock absorber for the knee. The IPFP is highly innervated by nocioceptive nerve fibers, including C fibers and the neuropeptide substance P, which may make this particular tissue especially prone to a sensitized state, resulting in a pain experience when the tissue is compressed during flexion or hyperextension. Their conclusions encouraged the consideration of not removing the IPFP during the TKA procedure as is common during this procedure.

Clockaerts, in 2010, found that IPFP is also a tissue capable of modulating inflammatory and destructive responses in knee OA.  So several positive benefits of the IPFP have been found beyond its obvious cushioning of forces to the anterior aspect of the knee.

Fat pad impingement can be easily confused with patellar tendonitis. However, patellar tendonitis tends to cause pain only at the patellar tendon, especially at the inferior pole of the patella. Fat pad impingement will cause pain on either side of the patellar tendon, where the fatty tissue sits. The pain may be worse with jumping, prolonged standing or any other position that causes the knees to hyperextend. Also, the area around the patellar tendon may be slightly swollen. Fat pad impingement is not associated with clicking, locking or instability.

Meneghini, in the J Arthroplasty 2007, found that patients whose fat pad had been removed during TKA were nearly twice as likely to experience postoperative pain. The IPFP has also been show to contain vascular endothelial growth factor.  The release of this factor after breeching the synovial lining of the fat pad during trauma or surgery may lead to vascular ingrowth or eventual scarring (Inflamed synovium produces inflammatory cytokines which promote the proliferation of fibroblasts and the production of collagen in synovial tissue, which can lead to tissue fibrosis).

Dr. Steadman of the Steadman Clinic in Vail, CO has reported that scarring of the anterior interval changes the mechanics of the anterior structures of the knee and may lead to refractory anterior knee pain.  Arthroscopic Anterior Interval Release successfully provides relief in this patient population. The anterior interval describes the anterior interval of the knee as the space between the infrapatellar fat pad and patellar tendon anteriorly, and the anterior border of the tibia and the transverse meniscal ligament posteriorly.  It extends from the lateral border of the medial meniscus to the medial border of the lateral meniscus. Normally, bridging scar tissue is not present in this area. The Structures of the anterior interval are typically mobile. If fibrosis courses from the fat pad to the transverse ligament it may lead to closure and dysfunction of the anterior interval. Closure of the interval causes decreased excursion of the patellar tendon in relation to the tibia.  The less elastic nature the IPFP, the more likely tethering of the patellar tendon may occur.  This tethering may cause stretching around the surrounding synovium during knee extension.  Tensioning/stretching of the synovium may lead to anterior knee pain and potential loss of full extension. 

Scarring of the anterior interval can be seen on MR finding seen on both T1 and T2 images differentiated from hemorrhage or edema.  Scarring has been shown to be prominent after previous surgical procedure (arthroscopy and open). Steadman has observed that little or no mobility occurred during interval closure in patients with IPFP fibrosis or scarring strongly suggesting decreased mobility of the fat pad when extending the knee.

To finish this part I introduction to the location, possible mechanisms, and clinical importance of the anterior interval, this is a highly innervated, vascular, and sensitive tissue!  Clinicians should give strong considerations to its’ mobility and irritability during rehabilitation of the knee.

Join me for Part II, where we will discuss clinical significance and potential treatment options!

 

Eric

Motion Guidanc

share this blog on socials

Proprioception

What are you focused on today?  Getting to work on time.  Finishing that house project that you’ve been banging away at for months now. Maybe just being a better parent or friend?

Now ask yourself what your clients are focusing on?  Are they focused on themselves?  Their pain? Their functional loss?  Where they hurt? Why they hurt?  How it affects them?

Often I find that our subjective reporting and evaluation procedures lead us down a very “internal” perception of body awareness.  While this can give us plenty of valuable information to help provide effective treatment, this can also carry over into treatment applications.  Is this leading us astray? 

I have often found in my clinical practice the dichotomy of asking people where they feel things vs how they are performing.  Making sense of the puzzle pieces of rooting through the information that is pertinent to each individual case and whether I should do something about it.  Should I strive to have each exercise, manually applied treatment, change of environment, and education piece be internalized, understood and accepted by the client?

Current and prior research findings, by such names as Wulf and Benjaminse, are giving us insight into how to improve our motor learning and body awareness outcomes by replacing internal focus with external focus during treatment applications. How a clinician presents rehabilitation, conditioning and retraining can have a marked effect on the desired outcome and not just the regimen or exercises themselves.  How the client responds to the feedback they receive may be just as, or even more important than the activity they are training with.

Instructions or feedback promoting an external feedback (i.e. goal oriented movement or the movement effect) have been shown to enhance learning, compared to those inducing internal feedback (focus on the body movement).  Numerous studies over the past decade, learning advantages of an external focus have been found consistently for a variety of skills, age groups, levels of expertise, and non-impaired as well.  Adoption of an external focus has ben shown to facilitate automaticity in movement control as well as movement efficiency, whereas internal focus tends to result in conscious control that constrains the motor system disrupt automaticity, and promote unnecessary muscular activity.  In short, internal focus may lead to self perceived concerns about performance and “micro-choking” events. Wulf thus argues that when internal focus is given to the client, reduced frequency should be more effective than feedback after every trial. In contrast, when external focused feedback is used, increased frequency may be more effectiveWulf did offer up in her critique of her own work in 2013 that there is still an argument that internal feedback is necessary and beneficial in early learning and there have been positive findings that novices perform effectively when their attention is directed to the skill rather than irrelevant/unnecessary secondary or external tasks. But she is also quick to point out approximately 80 experiments outlining the significant advantages of external relative to internal foci with only a “handful” yielding null effects.

Often the difficulty is attempting to translate this type of information into usable treatments in our clinics.  Just because we know what probably will help our clients improve better, faster, stronger; doesn’t always mean we have the resources or capabilities to implement this information. Benjaminse described several options for implementing EF into treatment regimens and even used descriptors in the recently published manuscript in JOPST to help clinicians.  Simple effects of changing verbiage to describe the same activity can make a huge difference in altering internal focus to external focus.  Some examples are as follows:

 

These examples are simple, yet effective ways to alter the effect of feedback that we give to our clients during training; trending more toward an external focus of movement.  Benjaminse also gives examples of real time feedback in the manuscript in the form of a Visual 3 D software called C-Motion, Inc. This type of technology is wonderful for allowing the client to gain immediate feedback for training purposes of motion.  The drawbacks of this type of tool are obvious though in both cost and space necessary to provide.  These specific factors are why I prefer the Motion Guidance advanced visual feedback system.  The advanced part refers the endless dynamic applications this system allows for.  Placing a mounted laser on any body part allows for the client to gain immediate feedback during motion. Adding delayed feedback and review can easily be done with a smartphone or tablet (insert endless aps here to use).  This system can provide a bridge between high tech and no tech and give clinicians options for providing an engaging source of external focus to the client.  And at less than $300 USD, it is affordable to most.

Regardless of the device, or lack of, that you chose to have in your treatment setting, the research trends are becoming clear.  Providing external focus has important implications for improving retention and performance. It has evidence that it speeds up the learning process, thereby enabling performers to achieve a higher level of expertise sooner. A potential solution specific to injury prevention may be grounded in neuromechanics. The training of conscious movement training into unconscious patterns to yield improved motor learning and strengthening to limit undesired movements or improve motor control into all movements.  That is our ongoing professional goal in athletic performance.

 

-Eric M. Dinkins, PT, MS, OCS, Cert. MT, MCT

share this blog on socials

Is Manual Therapy a Gateway Drug?

Manual Marijuana: Upper Cervical Spine

Manual Marijuana: Upper Cervical Spine

Living in the great State of Colorado has been interesting the past few years.  It was not too long ago that we voted as a State to allow each county to legalize marijuana for private use and for distributors to do so under scrutiny and taxation by the State.  As I travel domestically and internationally to teach therapy concepts, it is always a hot topic to discuss regarding our laws, and of course, discredit or educate the misconceptions and distortions of the truth.  Topics like: Pot is legal everywhere in the State! You can smoke and drive! If you are carrying more than the federal law on an interstate you still OK because the State passed a law! You can still consume and work because State law precedes employer policy or regulation! 

All of these are mistruths,  developed by hearsay and passed down from mistruth to mistruth.  But by far, the biggest topic is one of Marijuana being the “gateway drug”.  This is the idea that consumption originally is harmless and fun.  But over time, it leads to experimentation with other drugs, addiction, dependency, altered thought process, and crime.  All of these have two sides to the coin, but it got me thinking about my profession…Perhaps Manual Therapy is the “gateway drug” of physical rehabilitation?

There is pretty big debate currently on the effect of Manual Therapy and its place in rehabilitation medicine. In fact, several research articles have called into complete question of any efficacy of various manual treatments.  The Powers that Be have continually shown that manual medicine takes second fiddle to exercise, rest, or placebo effect.  So why continue with manual medicine techniques?

Any treatment of choice, but especially manual rehabilitation techniques were always (in my opinion), meant to be a treatment accelerator;  A way to get short-term immediate improvements that were enhanced by pain modulation by-products, self-empowerment by the client, and then return of functional/meaningful movement.  Now of course, I have seen some tremendous immediate results over the years that required nothing further (and this doesn't imply that the technique itself was the culprit.)  But most often, it has provided a gateway to move on to other procedures more quickly than without.

Does the patient need marinating? Is it necessary to affect the outcome? How much time are we spending marinating versus moving on to baking at 350? What we spend time on in clinic reflects it's importance to the patient. And uncooked food leads to further illness...

Does the patient need marinating? Is it necessary to affect the outcome? How much time are we spending marinating versus moving on to baking at 350? What we spend time on in clinic reflects it's importance to the patient. And uncooked food leads to further illness...

Too often I read research topics that, in methodology, are inherently biased and not clinically applicable.  Structured to mandate that a specific technique or treatment be repeated for a set number of repetitions and sessions to determine an outcome/effect.  I always end up asking myself “who would do the exact same thing for 4-6 visits regardless of outcome or result?”  The reality of clinic practice is that there are far too many factors (controllable and non-controllable) to expect that the situation or environment is the same each time you see a patient.  As an example, if we apply a manual based treatment, and there is a noticeable positive outcome, doesn’t it stand to logic that the next step is some type of progression or advancement?  In contrast, if there is a neutral or negative result, why would doing the same thing again make sense here?  Hence, back to the “gateway drug’ analogy.

Published research has given us significant insight into the vast array of physiologic changes that happen after manual medicine and other treatments.  But why stop there?  Maximize those short-term results by enhancing movement patterns, empowering the patient, performing functional activities or even non-specific exercise.  Start moving again!

There should not be battle between current research and past models of applied therapy.  Individuals who insist on swinging the pendulum to the opposite side are just as likely to see failures and pushback as their predecessors.  Lorimer Moseley was recently quoted at the recent IFOMPT 2016 “…the biopsychosocial model rejects the biomedical model because the medical model is not concerned with the person. But it does not reject the role of structural, biomechanical and functional disturbance of body tissue as potentially powerful drivers of protection.”

Embracing the middle of a multi-modal therapy has always seen success because it places the patient interest first…. psychology, empathy, hands on care, movement, pain.  We should stay open…to staying open

Stop condemning other models of therapy.  Rather, I employ my colleagues to understand that just because we may not know how something works, in the end…it worked for an individual…and that changed their life in a positive way. Explanations of techniques may need some adjusting, as from the biopsychosocial leaders we know we can positively or negatively influence patient’s view on their situation by the words we use. We don’t need to tell people we are going to put their rib back in place, or tell them their nerve is smashed because of their degenerative disc disease. We can use verbiage that alludes to an adaptable body, a resilient one, that may just need a push in the right direction. Just a puff.  Instead of abandoning techniques because their effects are non specific, we can change the framework of explanation, educating the patient that there are lots of ways their body can experience movement, and we want to attempt to do our best (with perhaps both manual therapy, specific or non specific exercise) to shape a context where the patient is succeeding in something meaningful to THEM (be it pain levels, specific task, or just strength).  If it doesn’t work, move on, try something else, be willing to be open…to being open. EVERY model of therapy, no matter what the basis or theory is, fails for someone.

Chad Cook was once quoted, “I am a manual therapist, but first and foremost, I am a physiotherapist.” Well said, Sir.  Sometimes we do not need understand exactly how we make success, but rather that we focus that we simply have successes.  And be willing to stay open to ideas and expansion of our treatment models.

 

Eric M. Dinkins

share this blog on socials

 

The Motion Guidance Concept

This blog is intended to discuss the overall concept of the Motion Guidance system.

To start with, lets discuss some relevant background research regarding proprioception, injury, learning, and how all this ties into the unique visual feedback system that your clinic can incorporate to help assist patients.

When considering how people learn, lets look at some general information about auditory, experiential, and visual learners. According to Bradford et al,  “Verbal learners, a group that constitutes about 30% of the general population, learn by hearing. They benefit from class lectures and from discussion of class materials in study groups or in oral presentations, but chafe at written assignments. Experiential learners - about 5% of the population - learn by doing and touching, and clinical work, role-playing exercises, and moot court are their best instructional modalities. Visual learners - the remaining 65% of the population - need to see what they are learning” (1)

Are we missing out by not making exercise more "visual" for our patients???

Are we missing out by not making exercise more "visual" for our patients???

Although this research applies to more of a classroom setting, we can extrapolate these results and apply them to the context of rehabilitation and motor learning. In lieu of this information, if goals in rehabilitating your patient are directed at teaching your patient about body awareness, movement, and understanding their movement strategies or position, we may be missing a crucial part of our education by not using visual feedback.

Research has also noted that the use of “external cues” for motor-learning (ie mirrors, targets, etc) are superior to the use of “internal cues” (ie instruction on how to move during a task) (2). Visual feedback with the Motion Guidance laser device offers a much superior external cue than targets or mirrors, as the feedback is instant and the cue is something the person can directly follow and understand, without the unnecessary cognitive processes of verbal instruction: they see it.

There has been much conversation on the need for compliance during home exercise programs, and during rehab in general as well. What might increase compliance? For a start, the activity needs to make sense as in what the purpose of doing it is, as well as be stimulating. Laser visual feedback covers both these areas: it offers an instant assessment of movement, while instantly allowing the visualization of progress and movement control. This may be especially important among the cohort of youth athletes, who are more likely to view exercise with laser visual feedback as a game, but the concept applies to everyone, as the majority of persons across all age groups are visual learners.

Our bodies have inherent mechanisms to allow us to know where we are in space. This includes vision, tactile sensation, and proprioceptive sensation. Laser guided visual feedback rehabilitation covers all grounds, to create a learning experience that is all encompassing of these mechanisms. Research has shown that our brain’s representation of our body undergoes changes when we are injured. This has been labeled “cortical smudging” or “altered-body mapping” by educators on the topic (3). Essentially, after injury, our discrimination of the injured body part is globally diminished, in all inherent mechanisms. This includes 2-point discrimination (being able to accurately feel and discern pin-prick sensation), as well as “joint positional awareness.” Joint Positional Awareness (JPE) is our ability to understand where our body is in space. Trevelean et al (4) have conducted numerous studies concluding that after whiplash, subjects have difficulty discerning their head position when tested with visual feedback from a laser pointer.

This phenomenon has also been noted in lower back pain patients (5), knee pain (6) as well as shoulder pain patients (7), and the concept applies to every body part. Can we use this knowledge to help us rehabilitate our patient’s condition? Yes! It is as simple as adding visual feedback to movement, and practicing joint positional awareness, motor control, and movement strategy. What can assist in changing the cortex, the brain’s “body-map”? Afferent inputs! These can be both positively or negatively reinforced, by practicing normal fluid movements, or maladaptive antalgic movements, respectively. If motor commands are not compatible with somatosensory feedback, and this continues persistently, we are left with a dysfunctional system under the influence of pain.

Our brain's understanding of our body is organized, and can undergo changes via neuroplasticity. 

Our brain's understanding of our body is organized, and can undergo changes via neuroplasticity. 

There are a boat-load of ways to influence proprioception. These may include manual therapy (tactile afferent input), taping (the research seems to conclude that, while not actually changing biomechanical interfaces, beneficial results exist due to a change in how we (our brain) “views” the body part under the influence of a novel stimuli. This doesn’t make it a sham per say, as any means in disrupting a pain full habitual experience can be beneficial to the person physically and psychologically. We can influence cortical reorganization by applying specific exercises that emphasize joint repositional awareness, and specific neuromuscular control (such as attempting to move a body part guided by visual feedback with a laser pointer, with the goal of precision and accuracy.) Again, it is as simple as practicing these tasks.  

Visual feedback training for lumbo-pelvic awareness: pelvic tilting

Visual feedback training for lumbo-pelvic awareness: pelvic tilting

Here is an example of using the Motion Guidance laser pointer device with cervical JPE:

 
 

The Motion Guidance concept is, by nature, a creative concept that can be applied to any body part, to yield instant positional awareness. Functions may include “static functions”, where the laser is kept centered while the body moves (such as keeping the laser centered while performing a "bird dog" exercise, or dynamic (such as moving the laser as far as possible upward and downward during lumbopelvic ROM exercise):

 
 

“dynamic functions” can be endlessly: a few examples would be neck in tracking patterns for cervical motor control, shoulder working on ROM, and lower chain loading control:

 
 

Beyond clinic use, clinicians can offer their patients home-units to train with visual feedback at home, based on the specific need of the patient, at the discretion of the care provider. This is where compliance may be enhanced, as the visual feedback training is innately understood, and requires no additional feedback other than instructions on what the goals are.


Motion Guidance patient packs can be purchased in bulk at discount rates, and offered to patients through your clinic, as a means of not only giving your patient a tool that may help retain between session learning objectives, but also gain clinic revenue.

 
Patient packs are sold in sets of 5, for clinicians to distribute to patients.

Patient packs are sold in sets of 5, for clinicians to distribute to patients.

 

For further video examples of applying the concept to cervical, shoulder, lumbar, lower chain, and general balance applications, brows our website’s HOW IT WORKS tab.

-Tal Blair, DPT

share this blog on socials


References:

1) Bradford, William C., Reaching the Visual Learner: Teaching Property Through Art (September 1, 2011). The Law Teacher Vol. 11, 2004. Available at SSRN: 

2) Wulf et al.  Frequent external-focus feedback enhances motor learning. Frontiers in Psychology. published: 11 November 2010 doi: 10.3389/fpsyg.2010.0019 

3) Schabrun et al. Smudging of the motor cortex is related to the severity of low back pain. ARTICLE in SPINE · APRIL 2015

4) Treleaven, et al. Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. J Rehabil Med. 2003 Jan: 35(1):36-43

5) Lee AS, et al Comparison of trunk proprioception between patients with low back pain and healthy controls. Arch Phys Med Rehabil 2010;91(9):1327e3 

6) Salahzadeh Z, Maroufi N, Salavati M, Aslezaker F, Morteza N, Hachesu PR. Proprioception in subjects with patellofemoral pain syndrome: using the sense of force accuracy. J Musculoskelet Pain 2013;21(4):341e9. 

7) Anderson VB, Wee E. Impaired joint proprioception at higher shoulder elevations in chronic rotator cuff pathology. Arch Phys Med Rehabil 2011;92(7):1146e51. 

Is "the core" a turn on, or a turn off?

“Nipples to Knees”, that’s how Tony Horton describes the area classically referred to as the core exercise group. We hear it far too often in the clinic setting, schools, and blogs.  Telling people to ensure they “engage their core” during or before exercise to help protect or reinforce their back. But this lays strong suggestion that people are just walking around and performing ADL’s without their core group being engaged.  This suggestion begs this question.  What is more normal?  Being pain free and moving while having subconscious core muscle sequencing?  Or being pain free and sustaining the world’s longest abdominal isometric and limiting fluid motion? 

There is research noting how hard the trunk stabilizers (identified as the obliques, rectus abdominis, QL, psoas, deep erecti spinal) are acting during activities like standing ,walking, and lifting. Its about 0 to 3-4% max voluntary contraction for standing and walking, and raises 2-3% for bending and lifting 15lbs (1). Doesn’t really line up for the patient crushing planks for 5 minutes because their “core is weak.”

If the goal for people with LBP is to have them eliminate their pain and return to their pre-back pain state, then what makes more sense? Being able to move freely with unconscious “core” control? 

Or, brace yourself…brace yourself!

Peter O’Sullivan has done several YouTube vids on this very topic and is blends pain science into his Cognitive Functional Therapy.  But in an attempt to over simplify what it takes to go from chronic back pain to living a normal life again can be broken down into three phases.

These include:

  • 1) Move.
  • 2) Gain strength and resiliency
  • 3) Move. 

In my opinion, it is imperative that these phases be completed in order.  Too often I find patients enter my clinic after episodes of back pain that have been told to NEVER bend, twist or lift again!  Stop moving and cope with your new life essentially.  Our first line caregivers have unfortunately fallen into an awful habit of condemning people to a life of early disability because of an acute subjective report.  Or worse, an MRI read. So after I spend 30 minutes with my patient on debunking the myth of their low back pain that was so helpfully planted by my fellow healthcare providers, I can then start on having them make their climb back to their pre-pain state and begin having them move their back- phase 1!

This is where I get my monies worth on the Motion Guidance system.  Anxiety about moving is a real barrier.  Adding visual feedback and goals gives a patient real time input on if and how they are starting to move their back. It also is more consistent with research in that, internal cues (like “draw in your belly and contract this or that while marching your legs on your back”) are not realistic, or transferrable, while external cues “keep the laser beam here, while reaching for this target” are dynamic, transferable, and visual.

Once ROM has been established, then a variety of strength and conditioning exercises can be applied. The therapist may have to identify if the patient is using an adaptive strategy (ie a strategy that is implemented by the body subconsciously or consciously that actually protects them at the given time, considering the level of real tissue damage or just perceived threat) or the patient may be using a maladaptive strategy (performing something to protect themselves, often consciously from fear avoidance, that actually impedes healing or progress). The former may be acceptable in the acute stages, but the end goal should be effortless movement, in variable contexts.

There are sooo many theories on how to get the body “back to normal”, and so very few proven to consistently work, it isn’t worth the ‘short blog’ time to begin to list em. Further, it is looking like “specific” core exercise focused on the tranny & friends are of no more benefit than “non-specific” exercise (2) - so we can simplify things a bit. But then, whatever you chose, phase 3 has to be completed.  Move, function, reach, lift, carry, sit, jump, stay fit.  Keep moving….

-Eric Dinkins

share this blog on socials

1) Eyal Lederman: The Myth of Core Stability. CPDO Online Journal (2007), June, p1-17

2) Saragiotto BT, et al. Motor Control Exercise for Non-specific Low Back Pain: A Cochrane Review. Spine (Phila Pa 1976). 2016.

 

Mini-Blog: Extension Intolerance

Sir Robin

Sir Robin

Painful extension can be a common finding in LBP patients, and localized extension related pain can come from a myriad of innervated tissue, though for non radicular pains facet sensitivity and possible disc annular sensitivity could be factors. 

Case report: Female, 30's, 1 year of unilateral back pain 2/10 constant and 8/10 after sports. She had ceased all exercise, though continued soccer 2x per week with consistent pain following each game. Her onset of pain was unknown, though she had episodes of same sided back pain during pregnancy. 

She had had an MRI indicating HNP at L5/S1 disc, though showed no sign of nerve damage (no sensation deficit, intact reflexes, no myotomal strength loss). 

Exam findings: AROM mild pain end range flexion with limited curve reversal, pain with any extension (unable to lie on stomach for more than 30 seconds), hypertonic and painful QL muscle on affected side, mild neural tension on affected side (slump test on affected yields mild increase in tension felt in back), poor lumbo-pelvic control and endurance during supine core exercise. 

Treatment: QL soft tissue work followed by isometrics (starting in side-lying, progressing to angled planks then on to regular side planks), neural tension progressions, core progressions, MWM (when prone laying became tolerant, we were able to achieve press-up extensions which felt much better with a "posterior innominate glide" during movement).

Visual feedback was utilized during core progressions with bent knee fall-outs  (keeping laser centered on ceiling during exercise), quadruped pointers (again keeping center once in pelvic neutral) as well as functional tasks. The patient had mentioned that hugging her husband was consistently painful (as her husband was tall and her back would hurt as it extended to hug).

Heres a quick vid on  functional task in pelvic neutral/slight post tilt during exercise:

pelvic positional awareness during functional tasks

At her 7th session, the patient was pain-free with ADL, had mild soreness after 1hr soccer game lasting only half an hour, and had returned to all exercise classes. 

Exercise with pelvic control is a great way to modify. It doesn't mean that it needs to be utilized for life, but as a means to allow tissue desensitization and continue fatiguing muscles and getting a work-out, as opposed to avoiding exercise because positions are painful. 

-T. Blair, DPT

share this blog on socials

Seeing the World Normal Again: an investigation into joint positional error.

What if everything that you saw with your eyes: every detail, every color every interpretation…was slightly wrong!?!  What if everything was the same shade of grey?  Or maybe just endless overlaps of grey? Everything seems perfectly normal from the outside, maybe through modification or adaptation, or even acceptance and avoidance. Well that might be exactly what is happening in the brain of some of your patients or clients!  And without the proper knowledge and resources, it may go unnoticed and untreated.

This blog is intended to help define and understand what joint position sense is (specifically at the cervical spine), how it might present in different conditions, and what the available resources are to help diagnose and treat it.

So let’s start with some definitions. 

What is proprioception and Joint Position Sense?

Proprioception can be defined as the unconscious perception of movement and spatial orientation arising from stimuli within the body itself in space.  An unconscious understanding of where body parts are, how they orient, and awareness of changes in location, whether large or small.  Several feedback mechanism act both together and independent of themselves to help give information to the central nervous system to enhance and maximize our body’s proprioception.  With regards to the head and neck area, there is a high density of muscle spindles in the small intrinsic musculature.  As a result, the neck musculature has an important role to play in postural control. An expansive number of experimental studies have demonstrated reduced postural control following neck muscle vibration or fatigue, and even ataxia following injection of local anaesthetic into the cervical tissues.  The dense network of mechanoreceptors in the soft tissues in this region not only controls multiple degrees of freedom of movements about each of its joints but, more importantly, gives the CNS information about the orientation of the head with respect to the rest of the body via direct neurophysiological connections to the vestibular and visual systems. Somatosensory information from the cervical region is the only region that has this direct access to the sense of balance and sense of sight.  There are extensive anatomical connections between neck proprioceptive inputs and vestibular inputs. If positional information from the vestibular system is inaccurate or fails to be appropriately integrated in the CNS, errors in head position may occur, resulting in an inaccurate reference for HNPS, and conversely if neck proprioceptive information is inaccurate, then control of head position may be affected.

To complement the muscle spindle feedback in position sense, the postural control system includes all the sensorimotor and musculoskeletal components involved in the control of two important behavioral goals: postural orientation and postural equilibrium. Postural orientation is the relative positioning of the body segments with respect to each other and to the environment, whereas postural equilibrium is the state in which all the forces acting on the body tend to keep the body in a desired position and orientation (static equilibrium) or to move in a controlled way (dynamic equilibrium). Postural control provides a stable body platform for the efficient execution of focal or goal-directed movements. The somatosensory, vestibular, and visual systems are the subsystems that provide sensory input to the postural control system.

Another subsystem, the Somatosensory Subsystem encompasses all of the mechanoreceptive information arising from the periphery which lead to the perception of pain, temperature, touch, and proprioception. The proprioceptive system of the cervical spine, in particular, is extremely well developed, as reflected by an abundance of mechanoreceptors, especially from the muscle spindles in the deep segmental upper cervical muscles. The muscle spindle system serves as the final common pathway for the regulation of the muscle stiffness required for various neuromuscular performances. Muscle spindle afferents appear particularly important, as they play the first violin in the proprioceptive ensemble, while other mechanoreceptors, such as the joint receptors and golgi tendon organs, fine tune the muscle spindle information, predominantly by reflex effects on the motoneurons.

The combined inputs from these systems give us our proprioception. And disturbances to the afferent input from the cervical region may be a possible cause of symptoms such as dizziness, unsteadiness, and visual disturbances, as well as signs of altered postural stability, cervical proprioception, and head and eye movement control.

How do we assess it?

Assessing sensorimotor impairment involves the assessment of proprioception – or joint position error (JPE) as it is termed in the neck – the assessment of oculomotor control and the assessment of postural stability. Research has demonstrated impaired control of the head and neck, altered eye movements and reduced postural control in both neck pain patients and whiplash injured patients. Proprioception is most easily assessed in the clinic using a laser attached to the head of the patient. The patient performs a physiological movement such as left cervical rotation with their eyes closed and attempts to return to the starting position – the neutral head position. This difference can be measured in centimeters to describe the joint position error. Postural stability in standing is very easily assessed in the clinic. A battery of balance tests from comfortable to narrow to tandem stances with eyes open and eyes closed should be included in the assessment of all neck pain patients. For the higher performing patient moving on to one leg stance and unstable surfaces would also be important. The cervical JPET tests one’s ability to relocate the head back to center after maximal or submaximal rotation in the transverse and sagittal planes. Per Treleaven’s research, clinical assessment cervical position sense can be assessed by using a laser pointer mounted onto a lightweight headband. Patients are asked to focus on the natural resting head position for a few seconds, sitting 90 cm away from a wall. With the eyes closed, they actively move the head and then try to come back to the resting position as accurately as possible. The difference between the starting and resting position of the laser beam on the wall can be measured in centimeters and then converted into degrees (angle = tan-1[error distance/90 cm]). Thus an approximately 7.1-cm error distance would translate to a meaningful error of 4.5° (as long as the subject is sitting 90 cm from the wall) and is called the joint position error (JPE). JPE can be assessed on return from all active cervical movements. Errors of greater than 4.5° are thought to suggest impairment in relocation accuracy of the head-neck. Patients might also demonstrate jerky or altered movement patterns, overshooting of the position in order to gain more proprioceptive feedback for the task, or “searching” for the position. Occasionally patients will also experience a reproduction of dizziness and/or unsteadiness with the task. 

Principles of motor control that address sensorimotor deficits in a more specific manner may be important for patients with complicated musculoskeletal problems. Coordination of movements is a core term in motor control and can be defined as the sensorimotor processes that organize and activate large and small muscles with the optimal amount of force in the most efficient sequence.

Cervical joint position sense can be retrained using a laser pointer mounted onto a headband with the light projected onto a wall, as described in the section on assessment. Patients practice relocating the head to a neutral position (guided by the laser beam) from their most difficult movement directions (for example, rotation to the right or following neck extension). This can then be performed with the eyes closed, using the laser for feedback with the eyes open on completion of the task. The task can be progressed by asking the patient to relocate the head position to different points throughout the range of motion (eg, left rotation 20°, 40°, and 60°) rather than the neutral head position. Performing these activities in more challenging standing positions can also be used as a progression for the exercises.

Cervical movement sense can be improved by moving the head, thus moving the laser, to trace patterns placed on a wall such as a figure-of-eight pattern. Patients can practice performing the task as accurately as possible, keeping the laser on the lines of the pattern. In both exercises accuracy should be encouraged at the outset; but once this has been established, the patient can attempt to perform the activities as quickly and as accurately as possible.

What’s the risk in not assessing cervical JPE?

The training of neck position sense is aimed at better perception of body posture, dissociation between body parts, and better awareness of the body's position in space, especially improvement of the patients' awareness of the head-neck and shoulder girdle posture, and is dependent on proprioceptive, visual, auditory, and vestibular cues.

Less accurate and less consistent repositioning performances were observed in fatigue relative to No fatigue condition, as indicated by increased absolute and variable errors, respectively. These results evidence that cervical joint position sense, is degraded by muscular fatigue. These observations are consistent with the existing literature reporting degraded proprioceptive acuity following muscle fatigue induced at the ankle,

As cervical joint position sense is considered to be predominantly signaled by muscle spindles, the effect of muscular fatigue on the muscle spindle system could provide a plausible neuro-physiological mechanism of the adverse effects of muscle fatigue on cervical joint position sense reported in the present study. This hypothesis is supported by evidences from previous animal studies of a modification of the discharge patterns of muscle spindles with muscle fatigue. Therefore, clinical implication stems from the concomitant observations of a reduced neck muscles strength and endurance capacity in patients with neck pain disorder would likely demonstrate impaired cervical proprioception and potential early global fatigue compared not normal. What we do know is the degraded cervical joint position sense observed with fatigue could contribute to the deleterious effects of cervical muscular fatigue on postural control during quiet standing as recently reported in the literature.

Another altered proprioceptive systems include gait. Martini (Archives of Phys Med 2011) described that concussed individuals displayed with significant differences in medial-lateral Centre of Mass displacement and displacement velocity were noted as well as the concussed group moved less and at slower speeds during testing and this conservative gait strategy appeared to remain in subsequent years.  This may present as impaired motor planning, a possible effect of impaired body awareness or normalization and is suggestive that post-concussive individuals may have alterations in body awareness and brain function that could persist for years and have the potential to influence work and health status and quality of life. This strikes the question of “Are we seeing the World after normal after certain injuries?”.  Or have we simply done what the human body is so good at?  Have we just adapted the way we see and feel to make a new normal? And what might be even more compounding is the trend of first line physicians in the U.S. to have the concussed patient simply rest until magnified symptoms resolve. Or worse yet, have standardized or computerized tests, without implementation by a trained rehab professional, dictate when an individual is ready to return to sport or work duties.  Recently in the AJSM, Brooks et al. in 2016 suggest that it is unclear if standard clinical tests have the sensitivity to detect subtle deficits in neurocognitive function.  And that changes in both neurocognitive and proprioceptive function may be a possible explanation for increased risk of injury after return to sports.  They found that concussed athletes have increased odds of sustaining an acute lower extremity musculoskeletal injury after return to play compared to non-concussed individuals.

And if the rested individual is able allowed to return to function without full examination, with mild symptoms of neck pain, this is what we know. Clinical Presentation Patients with neck pain seem to have a poor awareness of their head-neck posture, and some indeed complain about “a wobbling head,” which may be resultant of impaired cervical position sense.  Specific to the neck and head, several studies have documented the alterations in cervical Joint Position Sense after whiplash and with neck pain. De Vries et al in Manual Therapy in 2015 found that JPS error is generally higher in the neck pain population that in a control group of similar size.   And that JPS error was velocity dependent.  At higher motion speeds, more JPS error was noted as well as a correlation intensity of neck pain and presence of JPS error.  And we are potentially send these individuals back to sport or full function and work duties?  It is my strong opinion that we must properly assess JPE before we discharge and return to pre-morbid functional levels. Especially when Clinical Research Relocation tests that either relocate the natural head posture or the head to a set point in range have most commonly been used to verify poor awareness of the head-neck region in patients with neck pain to reflect impaired cervical position sense. These methods address a patient's ability to consciously indicate when a pre-specified position has been reproduced. Impairments have been demonstrated by these methods in subjects with neck pain of both idiopathic and traumatic origin (ie, whiplash injury).

Even if we do rehabilitate to the best of our ability and resources, we can’t ensure re-injury won’t occur.  For example, Nordstrom in 2014 found that footballers who sustained a concussion were more prone to injury that the rest of their teammates.  And this persisted for 1 year suggesting the presence of residual effects from the initial analysis.  The rehab protocols for testing JPE were not mentioned in this case however.

In other injury populations, the relationship between neurocognitive function and injury may be established.  Swanik, (AJSM 2007) found decreased reaction times, processing speeds, and visual-spacial disorientation may expose athletes to injury prone situations.  Perhaps testing normal, but still “seeing the World differently”, may lead to difficulty with interpreting and negotiating information when challenged with unanticipated events; momentarily leading to alterations of proper motor programming or typical muscle activity, effectively diminishing the dynamic restraint capabilities…commonly referred to as decreased/loss of situational awareness.  This might be taking some leaps to connect the dots…but if we aren’t properly testing for JPE then we cannot rule this connection out.

Nordstrom also found that a laser method for assessing JPSE had good test-retest reliability and a strong correlation with an ultrasound technique for measuring JSPE.  However, most outpatient clinic settings are not likely to have a reliable piece of laser equipment that can be used to properly and accurately test for JPS error. 

The Motion Guidance large strap and perpendicular mount can be used to assess "JPE"

The Motion Guidance large strap and perpendicular mount can be used to assess "JPE"

So if we can’t test for cervical JPS, then we aren’t directly treating it either.  And if we aren’t directly assessing or treating it, then we as rehabilitation specialists have to concede that it may go unnoticed and therefore be a potential and plausible outlier of increased risk of any future injury to that individual.  This is one reason why I prefer the Motion Guidance visual feedback system. This system allows any practitioner to turn their clinical setting into a immediate testing and training ground for multiple body parts including cervical JPS.  The system has a highly durable, two sided flag that has 2 targets standardized to Jull and Treleaven’s research.  One smaller target calibrated at 90 cm.  And a larger, multi-colored target calibrated at ~152 cm.  Another unique aspect of the MG device is found in that the mounting strap can be placed over the eyes of the patient to prevent the subject from attempting to use extra visual feedback to more accurately pass a JPS test.

Whatever you decide to your use your clinic, please….just decide….to actually use it!

Eric M. Dinkins, PT, MS, OCS, Cert MT. MCTA

share this blog on socials

References

Treleaven, et al. Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. J Rehabil Med. 2003 Jan: 35(1):36-43

Gong, Wontae. Effects of cervical joint manipulation on joint position sense of normal adults. Journal of Physical Therapy Science 2013;  25:721–723.

Haavik H, and Murphy B. Subclinical neck pain and the effects of cervical manipulation on elbow joint position sense. Journal of Manipulative and Physiological Therapeutics 2011; 34(2):88-97. doi: 10.1016/j.jmpt.2010.12.009

Bigland-Ritchie B, Rice CL, Garland SJ, et al. Task-dependent factors infatigue of human voluntary contractions. In: Gandevia SC, Enoka RM, Mc-comas AJ, et al, eds. Fatigue. New York, NY: Plenum Press; 1995:361–80.2.

Bjo¨rklund M, Crenshaw AG, Djupsjo¨backa M, et al. Position sense acuity isdiminished following repetitive low intensity work to fatigue in a simulatedoccupational setting. Eur J Appl Physiol 2000;81:361–7.3.

Carpenter JE, Blasier RB, Pellizzon GG. The effects of muscle fatigue onshoulder joint position sense. Am J Sports Med 1998;26:262–5.4.

Lee HM, Liau JJ, Cheng CK, et al. Evaluation of shoulder proprioceptionfollowing muscle fatigue. Clin Biomech 2003;18:843–7.5.

Voight ML, Hardin JA, Blackburn TA, et al. The effects of muscle fatigue on and the relationship of arm dominance to shoulder proprioception. JOrthopSports Phys Ther 1996;23:348–53.6.

Allen TJ, Proske U. Effect of muscle fatigue on the sense of limb position and movement. Exp Brain Res. 2006;170:30–8.7.

Brockett C, Warren N, Gregory JE, et al. A comparison of the effects of concentricversuseccentricexerciseonforceandpositionsenseatthehumanelbow joint.Brain Res. 1997;771:251–8.

Armstrong BS, Peter JM, Maynard W: Head and neck position sense in whiplash patients and healthy individuals and the effect of the cranio-cervical flexion action. Clin Biomech 2005, 20:675-684.

 Heikkila HV, Wenngren B: Cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury. Arch Phys Med Rehabil 1998, 79(9):1089-1094. 

 Lee H, Teng C, Chai H, Wang S: Test-retest reliability of cervicocephalic kinesthetic sensibility in three cardinal planes. Man Ther 2006, 11(1):61-68.

Rix GD, Bagust J: Cervicocephalic kinesthetic sensibility in patients with chronic, nontraumatic cervical spine pain. Arch Phys Med Rehabil 2001, 82(7):911-919.

Receding Hair Lines and Joint Lines: A Process of Life

 

Osteoarthritis (OA) is the most common joint disorder in the United States. Symptomatic knee OA occurs in 10% men and 13% in women aged 60 years or older (1). An estimated 4 million adults in the US are trotting on bionic knees, and the rate of TKAs has doubled in the last decade and continues to be on the rise (2). In reality, knee arthritis is a process of aging, its inevitable, and will happen just like a receding hair-line. Even if you are this guy:

Impeding hair line

Impeding hair line

Of course, there are always options:

Of course, there are always options:

 

But is a receding joint necessarily in doom? In Paul Dieppe’s article (3) he demonstrates the disconnect between pain and radiographic findings, and the problem that the “radiographic finding” can give us the disease and is pushing us toward a much overzealous surgical fix.

“We should be looking for low tech, inexpensive, simple ways of reducing the burden of illness with respect to pain, limitation of activities, and participation in life by older people. If we're going to progress in this field, I believe we must make these paradigm shifts.”

–Paul Dieppe

What Matters: Pain?

What seems to matter most is the amount of pain, and the age of the person (perhaps the older population has been to the doc for an image they feel due for a TKA?) as McAlindon et al demonstrated that knee pain and age are more important determinants of functional impairments in elderly subjects than the severity of knee OA as assessed by radiographic features (4).

To put it simply, it seems pain is to be implemented, not the radiographic features, in the diagnostic category of knee OA. Jordan et al. also concluded that knee pain severity was more important than radiographic knee OA severity in determining disability (5).

One study of over 2000 persons shows about 44% of people have radiographic OA, and about 20% have symptoms. The same study shows quad weakness associated with pain, but not radiographic knee OA (6). Other authors point to the need to look toward quad strength and motor control as opposed to a massive operation, in light of the pandemic arthroplastic surge. Brandt reminds us that OA is not a cartilage disease alone, but involves the whole joint. OA is about bone, synovium, and capsule as much as if not more than cartilage (7). I think this is an important way to view things, and can be used in explanation to patients: there is more to the picture than just the picture (x-ray).

Receding Cartilage

Studies have indicated that prior to cartilage deterioration, the knee shows signs of inflammation and medial meniscus damage early on, inflammation (Hoffa synovitis and effusion synovitis), along with meniscal “extrusion.” Furthering Brant et al’s findings (8). This should give us reason to suggest frequent movement/cycling/etc to our patients, as a prevention measure, to minimize inflammation. 

When comparing prevalence among differing sex, women seem to be more OA-prone, both in pain reports as well as radiographic findings. One study shows that out of a group over 600, women showed slightly higher radiographic OA than men (35 % vs 31 %) but twice as many women reported knee pain than men. Over 60% of persons over 60 had radiographic knee OA (9). 

The consensus is clear that as age and OA findings have a linear relationship, which does not come as a surprise. But remember, OA does not equal pain. The Framingham Osteoarthritis Study found that 10% of people aged 63 years and over had symptomatic knee OA (pain) in the presence of radiographic changes (10). In people with severe OA, it seems about half report pain (11). Although some studies find the link of reported pain and OA severity less clear, large scale studies (4000 subjects) finds a clear relations between the roughly 40% of persons with radiographic OA and pain (12). Even in these studies, 60% of the persons with radiographic OA did not have pain. Further, can the 40% improve? If so, their “radiographic” OA isn’t changing….

Factors in Joint Stress

When considering factors with joints and stress, obesity is a topic often broached. Some really interesting things are brought up the “lower extremity review” regarding obesity and knee OA. In looking at WOMAC scores (questionnaire on ADLs and pain), obese people had higher risk for reporting bilateral knee pain, EVEN in persons with little to no “radiographic OA” changes (13). This indicates that the pain felt can be variable and not dependent on changes in the knee, even in knees you may think must be over-stressed.

Dr Weiss of LE review found that though her extensive research, knee pain does correspond to physical joint changes, but individuals with higher BMIs experience more pain, regardless of the amount of radiographic OA (14). Again this information begs the psychosocial implications of knee pain, however reasons might be explained by physiological change as well: one suggestion was that obese people have more pain in their joints due to an increase in “leptin” which modulates inflammation, as chronic low levels of inflammation are correlated with Obesity (15).

It may be proper to educate not only on weight loss, but also anti-inflammatory diet.

Further, there may be a lot of knee-related benefits that come from weight loss, not only decreased joint loading (think increased mobility, increased mood, positive outlook, increased activity, slimmer jeans and so on).  

Loading & Biomechanics

When considering specific loading, we look no further than upon the medial condyle to enlighten us, as the medial condyle takes the majority of loading in the knee. Kumar et al. showed that knee OA subjects have high medial contact loads in early stance, and greater knee adduction moment (KAM). They also demonstrate greater static and dynamic varus of the knee.

In the biomechanics world, KAM (knee adduction moment) has been a topic of discussion, and thus effort to change it dynamically has been suggested. KAM is the torsion force which adducts the tibia on the femur. The magnitude of KAM during walking has been related to tibial bone changes, as well as OA severity (17,18).

Some suggest altering gait to reduce KAM: one being the “toe out” angle of the foot: apparently toe out stance during initial contact and the first 50% loading doesn’t really affect KAM, though in the last 50% of stance, toe-out position can reduce KAM (19, 20). Other biomechanical factors include lateral trunk lean (which in magnitude has shown to be related to disease severity as well as reported pain) (21, 22). Though because lateral trunk lean actually orients the ground reaction force closer to knee joint center and lessens the medial compartment loading and KAM, we are thinking this is a compensation…this always brings up the notion that when we analyze a patient's gait, we are only seeing how they move in pain (ie the pain itself is influencing what we are seeing, not necessarily the other way around). These strategies may be adaptive or maladaptive.

Other strategies to reduce KAM include increasing hip internal rotation and adduction, and slight knee flexion, to get the knee physically closer to the GRF (23). Subjects instructed to walk with their knees as close together as possible (to reduce dynamic varus) showed major decrease in KAM magnitude (24, 25). Other research recommends treadmill walking and an incline greater than 5% to significantly decrease frontal knee loading (26).

Even delving into the patient's personal fashion sense can provoke load changing solutions: what shoes we wear also affect dynamic knee stress, as Ho KY et al points out in noting an increase in patella-femoral joint stress in women wearing heels due to higher knee extension moments and knee flexion angles (27).

One clinical trial states “Gait retraining reduced the first peak KAM by 20% (p<0.01) post-training as a result of a 7° decrease in foot progression angle (i.e., increased internal foot rotation), compared to baseline (p<0.01).” though the N is only 7, and it is not clear what instruction/method helped the patients gait chance (what they did differently) or if they retained this long term (28).

It seems the logic of all this KAM research is this: we see a lot of medial joint deterioration on images, this is probably the cause of pain, joint deterioration must be associated with high loads on the medial joint, so we should reduce loads at the medial joint and disperse them through out the joint with by changing GRF. So we will tell people to walk in ways that have the least load at the medial knee, so we don’t cause more damage here. It seems logical, but to me more a tactic to take a break from the consistent loading that become associated with pain. It is important to note there are many factors beyond mechanical loading that can affect pain: Central sensitization has also been though to contribute to the more painful cases of knee OA, as the radiographic evidence can also be disproportionate (29).

From what I can gather from the knee OA research is that there is a high prevalence of radiographic knee OA with a linear relationship to our age. Joint space and cartilage health can be factors in whether the person has pain, but are not alone indicative of pain. People with more “bone on bone” tend to have more pain, but not overwhelmingly. Obese people tend to have more pain, regardless of their “bone on bone”. Changing loading can affect how much pain a person has, despite the “BOB” extent. It makes sense to me to lessen the load on any sensitive tissue temporarily, change loading in a way that is functional and appropriate for the patient, and allow the “painful area” to become more resilient, and less sensitive. To me, the mechanisms of this outcome are part mechanical via altering the load, while allowing exercise and movement and life to resume, part mechanical in the sense that having stronger more resilient structure surrounding the painful and “threatened” knee allow for reductions in true joint stresses, as well as the patients psychological benefit from being able to resume some sort of strengthening to the area despite their belief that their joint is “no good”, and in part due to the patient having a plan to return their knee to a more useful state. Graded exposure can be huge here: if a patient has severe pain after 5 minutes of walking, get them timing themselves for 2 minutes, 5 times per day. If going up a step seems a nightmare, have the patient unload themselves somehow: elbows on a table practicing a 2" step, or just pushing 50% into the step up motion. Allow progressions as the patient stays sub-threshold of a “flare up” and make them aware of their progressions.

As the patient sees some sort of progress (even if that is open-chain quad strength improving) they are gaining potential to fall into the demographic of “asymptomatic radiographic knee OA”. The fact that there exists such a category should be bookmarked in your patients thought process. Your pre-TKA patients will undoubtedly have a neighbor, Sally or Bill, that can't stop talking on the greatness of their new knee. Even with the patients that undergo surgery and are smiling, it still doesn’t prove that their intervention was implemented in their result: interestingly placebo surgery was no different than actual arthroscopic debridement in 180 patients with pain: in both, the majority of people got better (30)! Furthermore, some research comparing non-op and operative patients (regarding PFPS) show persons (N=56) undergoing knee arthroscopy and exercise is no better than exercise alone for people with PFPS (31)! I am not suggesting that the TKA be removed from the menu, but that there be some hope in persons who have been told they have radiographic knee OA, have pain and decreased function, to significantly improve their condition and resume a life, without removing a small portion of their lower extremity. 

While the massive amount of research can be daunting, and somewhat conflicting and confusing, I think the take home point is to decrease the concept that cartilage deterioration itself is a disease that once present is detrimental to life and function, that we can temporarily change loading, both mechanically and in terms of dosage to make tissue more accepting and less painful (regardless of the Kellgren and Lawrence system findings) as well as change the way a person perceives their knee (although this can be difficult after the “nocebo” effect from white jackets pointing to thin joint lines).

You can use visual feedback cues to change loading strategy, and modify or promote ROM.

Some applications include:

  • Obtaining terminal knee extension in those lacking, for improved mechanical quad functioning during gait

  •  Promoting loading awareness, by improving joint positional sense during closed chain exercises (if a person can only load one way, and the current route is paved in sensitive tissues, then they need to find alternatives at least temporarily)
  • Adding a visual component to simple exercise: balance reaches, hip stability, squatting, and any component I feel the patient has potential to gain more control of.

More importantly, they can see this change in motor control and positional awareness!

 

 

-Tal Blair, DPT

share this blog on socials


1)Yuqing Zhang et al. Epidemiology of Osteoarthritis Clin Geriatr Med. 2010 Aug; 26(3): 355–369. doi:  10.1016/j.cger.2010.03.001

2)Weinstein AM et al. Estimating the burden of total knee replacement in the United States. J Bone Joint Surg Am. 2013 Mar 6;95(5):385-92. doi: 10.2106/JBJS.L.00206.

3)PAUL A. DIEPPERelationship Between Symptoms and Structural Change in Osteoarthritis. What Are the Important Targets for Osteoarthritis Therapy?© 2004. The Journal of Rheumatology Publishing Company Limited. 

4)T. E. McAlindon et al. “Determinants of disability in osteoarthritis of the knee,” Annals of the Rheumatic Diseases, vol. 52, no. 4, pp. 258–262, 1993. 

5)J. M. Jordan, G. Luta, J. B. Renner et al., “Self-reported functional status in osteoarthritis of the knee in a rural southern community: the role of sociodemographic factors, obesity, and knee pain,” Arthritis Care and Research, vol. 9, no. 4, pp. 273–278, 1996

 6) Shigeyuki Murak et al. Quadriceps muscle strength, radiographic knee osteoarthritis and knee pain: the ROAD study BMC Musculoskeletal Disorders 201516:305

7) Brandt KD et al. Quadriceps strength in women with radiographically progressive osteoarthritis of the knee and those with stable radiographic changes. J Rheumatol. 1999 Nov;26(11):2431-7.

8) Roemer FW et al. What comes first? Multitissue involvement leading to radiographic osteoarthritis: magnetic resonance imaging-based trajectory analysis over four years in the osteoarthritis initiative. Arthritis Rheumatol. 2015 May;67(8):2085-96. doi: 10.1002/art.39176.

 9) Lan T. Ho-Pham et al., Prevalence of Radiographic Osteoarthritis of the Knee and Its Relationship to Self-Reported Pain. Published: April 10, 2014 DOI: 10.1371/journal.pone.0094563

10) D. T. Felson, A. Naimark, and J. Anderson, “The prevalence of knee osteoarthritis in the elderly. The Framingham Osteoarthritis Study,” Arthritis and Rheumatism, vol. 30, no. 8, pp. 914–918, 1987. 

 11) Hannan MT et al. Analysis of the discordance between radiographic changes and knee pain in osteoarthritis of the knee. J Rheumatol. 2000 Jun;27(6):1513-7.

12) Laxafoss E et al. Case definitions of knee osteoarthritis in 4,151 unselected subjects: relevance for epidemiological studies: the Copenhagen Osteoarthritis Study. Skeletal Radiol. 2010 Sep;39(9):859-66. doi: 10.1007/s00256-009-0856-x. Epub 2010 Jan 30.

13) Kellgren JH, Lawrence JS, eds. The Epidemiology Of Chronic Rheumatism: Atlas of Standard Radiographs of Arthritis. Vol 2. Oxford: Blackwell Scientific; 1963.

14) Weiss E. Knee osteoarthritis, body mass index and pain: data from the Osteoarthritis Initiative. Rheumatology 2014 Jun 17.

15) Elbaz A, Debbi EM, Segal G, et al. Sex and body mass index correlate with Western Ontario and McMaster Universities Osteoarthritis Index and quality of life scores in knee osteoarthritis. Arch Phys Med Rehabil 2011;92(10):1618-1623.

16) Kumar et al. Knee joint loading during gait in healthy controls and individuals with knee osteoarthritis. Feb 2013: Vol 20, Issue 2, Pgs 298-305

17) Jackson BD, Teichtahl AJ, Morris ME, et al. The effect of the knee adduction moment on tibial cartilage volume and bone size in healthy women. Rheumatology 2004;43(3):311-314.

18) Miyazaki T, Wada M, Kawahara H, et al. Dynamic load at baseline can predict radiographic disease progression in medial compartment knee osteoarthritis. Ann Rheum Dis 2002;61(7):617-622.

19) Lynn SK, Costigan PA. Effect of foot rotation on knee kinetics and hamstring activation in older adults with and without signs of knee osteoarthritis. Clin Biomech 2008;23(6):779-786.

20) Lynn S, Kajaks T, Costigan P. The effect of internal and external foot rotation on the adduction moment and lateral-medial shear force at the knee during gait. J Sci Med Sport 2008;11(5):444-451.

21) Hunt MA, Wrigley TV, Hinman RS, Bennell KL. Individuals with severe knee osteoarthritis (OA) exhibit altered proximal walking mechanics compared with individuals with less severe OA and those without knee pain. Arthritis Care Res 2010;62(10):1426-1432.

22) Hunt MA, Birmingham TB, Bryant D, et al. Lateral trunk lean explains variation in dynamic knee joint load in patients with medial compartment knee osteoarthritis. Osteoarthritis Cartilage 2008;16(5):591-599.

23)Barrios J, Crossley K, Davis I. Gait retraining to reduce the knee adduction moment through real-time visual feedback of dynamic knee alignment. J Biomech 2010;43(11):2208-2213.24) Fregly BJ, Reinbolt JA, Rooney KL, et al. Design of patient-specific gait modifications for knee osteoarthritis rehabilitation. IEEE Trans Biomed Eng 2007;54(9):1687-1695.

25) Schache AG, Fregly BJ, Crossley KM, et al. The effect of gait modification on the external knee adduction moment is reference dependent. Clin Biomech (Bristol, Avon) 2008;23(5):601-608.

26) Henry Wang. Incline walking: An offloading option for patients with knee OA. LER. Aug 2014

 27) Ho KY et al. The influence of heel height on patellofemoral joint kinetics during walking. Gait Posture. 2012 Jun;36(2):271-5. doi: 10.1016/j.gaitpost.2012.03.008. Epub 2012 Apr 19

28) Shull PB et al. Six-week gait retraining program reduces knee adduction moment, reduces pain, and improves function for individuals with medial compartment knee osteoarthritis. J Orthop Res. 2013 Jul;31(7):1020-5. doi: 10.1002/jor.22340. Epub 2013 Mar 12.

 29) Lluch E et al. Evidence for central sensitization in patients with osteoarthritis pain: a systematic literature review. Eur J Pain. 2014 Nov;18(10):1367-75. doi: 10.1002/j.1532-2149.2014.499.x. Epub 2014 Apr 3.

30) Moseley JB et al.  A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2002 Jul 11;347(2):81-8.

 31) Jyrki A Kettunen et al. Knee arthroscopy and exercise versus exercise only for chronic patellofemoral pain syndrome: a randomized controlled trial. BMC Medicine20075:38 DOI: 10.1186/1741-7015-5-38

Psoas Conundrum...

Psoas...It's what's for dinner.

Psoas...It's what's for dinner.

 

Mmmmmmm steak!  Recently my wife and I made the family menu transition to Pescaterian.  That one step above vegetarian that allows you to keep some type of meat in your diet…fish.  Now, while I really like salmon, there is something that just doesn’t satisfy like a good, thick, Psoas Major with béarnaise sauce dripping from the slightly crusted surface.  Yep.  That’s right.  Psoas Major.  In a cow, Psoas is the largest, thickest portion of what is termed tenderloin.  In humans, Psoas Major is a fusiform muscle of approximately 16 inches in the adult.


It has a superficial and deep layer; the former arises from the transverse processes of L3-5 and the brim of the lesser pelvis. The superficial layer arises from the lateral surface of the lower thoracic and all lumbar vertebrae plus their associated discs. These two muscle layers traverse downward and laterally under the inguinal ligament and over the iliac fossa to become continuous with the iIiacus muscle. In humans, the psoas is a combination of fast and slow twitch fibers. Regarding Psoas minor, this exists in only 50% of humans. It is a long slender skeletal muscle running anterior to the medial border of psoas major and is a weak flexor of the hip. Psoas minor arises from the facets of T12-L1 and inserts into the iliopectineal eminence. Fibers also stretch and attach to the deep iliac fossa with fibers to the inguinal ligament. The remaining portion of the group is combined with Iliacus. This flat wide muscle fans from the borders of the iliac fossa downward to blend with fibers of the psoas muscle(s) before attaching to the lesser trochanter.

As Psoas histologically has a combination mix of fast and slow twitch fibers, Psoas muscle (PM) function with regard to the lumbar spine (LS) is disputed. Electromyographic studies attribute to the PM a possible role as stabilizer. Anatomical textbooks describe the PM as an LS flexor, but not a stabilizer. According to more recent anatomical studies, the PM does not act on the LS, because it tends to pull the LS into more lordosis by simultaneously flexing the lower and extending the upper region, but due to the short moment arms of its fascicles, this would require maximal muscular effort and would expose the LS motion segments to dangerous compression and shear. These findings would indicate that the described opposite action of the PM on upper and lower LS regions, performed passively and requiring minimal muscular effort, may serve to stabilize the LS in an upright stance. It has been demonstrated that a vertically placed elastic metal strip, modelled into a lordotic configuration to imitate the LS, will be brought into more lordosis, with maintenance of vertical position, if a string fastened at its upper end is pulled downward in a very specific direction. Conversely, any increase of lordosis of the strip brought about by vertical downward pushing of its top, will be stabilized by tightening the pulling string in the same specific direction. As this direction corresponded with the psoas orientation, the experiments show that the PM probably functions as a stabilizer of the lordotic LS in an upright stance by adapting the state of contraction of each of its fascicles to the momentary degree of lordosis imposed by factors outside the LS, such as general posture, general muscle activity and weight bearing. The presence of multiple PM fascicles, all of about equal length, and attaching to all LS levels, facilitates this function. Some researchers and anatomists still refer to the hip flexor muscle complex as one unit or as the iliopsoas. The psoas muscle differs from the iliacus in that it has a different architecture, innervation and more importantly, a different function. A better understanding of the role of the psoas muscle and its impact on lumbopelvic stability may improve the clinical management of individuals suffering from lower back pain. So with understanding that Psoas might be more apt to be viewed as a stabilizer vs. a mover, then why are we stretching Psoas or performing soft tissue mobilization (espcially since this is ridiculously painful for the client and likely just compresses that large piece of tendeloin that I just put into my small intestine about 2 hours ago)?  And trying to get a muscle to stretch by combining hip extension with lumber flexion is close to impossbile considering that according to Park and Hodges in a 2013 study that Recruitment of discrete regions of the psoas major and quadratus lumborum muscles is changed in specific sitting postures in individuals with recurrent low back pain.  They found that in individuals with LBP, that Psoas was tonic enough to have a potential extensor moment, even in sitting.  So if sitting can’t shut off Psoas Major in our clients, then how do we expect to stretch against that force in any other position? 

Nachemson showed that the psoas major was active during upright standing, forward bending, and lifting. These observations prompted the inference that the psoas major may function as a lumbar spine stabilizer. Others have since proposed and found evidence for various roles that the psoas major may play with respect to lumbar spine stability and movement. These roles include psoas major being a flexor of the lumbar spine on the pelvis, a lateral flexor of the lumbar spine, a stabilizer of the lumbar spine, stabilizer of the hip, power source for bipedal walking and running, and controller of the lumbar lordosis when supporting difficult lumbar load.

Yoshio et al. used cadavers to analyze the psoas major in its dynamic phase (as a flexor of the hip joint) as well as in its static phase (involving fixation of the hip joint to maintain a sitting or standing position against gravity). Their results suggest that the psoas major works phasically: as an erector of the lumbar vertebral column, as well as a stabilizer of the femoral head onto the acetabulum (from 0°–15°); exerting decreased stabilizing action, in contrast to maintaining the erector action (from 15°–45°); and as an effective flexor of the lower extremity at the hip joint (from 45°–60°). They further concluded that the function of the psoas major as a hip stabilizer is overshadowed by its action of stabilizing/erecting the lumbar vertebral column.

The electromyographic work of Basmajian was the first to investigate the role of the iliopsoas. He concluded that the psoas major could not be separated from the iliacus with regards to their collective action of a hip joint flexor. Keagy et al.performed electromyographic studies on the psoas major in five patients with wire electrodes placed directly into the muscle. Recordings made during various activities indicated that psoas played a significant role in advancing the limb while walking and in controlling deviation of the trunk when sitting. The action of the psoas in rotation, abduction, and adduction of the hip was slight and variable.

Over the last decade, new insights into muscle function and the role of muscles in providing dynamic stability have emerged. Some muscles may have stabilization of the lumbosacral spine as their primary role, while others appear to have multiple roles and these multiple roles may be dependent upon spinal position and the loads being transmitted to the spine (i.e. low load vs. high load).

Recent research on lumbar musculature and how it relates to individuals suffering from lower back pain has progressed through the use of advanced imaging techniques. Dangeria and Naesh conducted a clinical prospective cohort study examining the cross-sectional area of the psoas major in healthy volunteers and subjects with unilateral sciatica caused by a disc herniation. These authors demonstrated that in most patients with a lumbar disc herniation there was a significant reduction in the cross-sectional area of the psoas major on the affected side only and most prominently at the level of the disc herniation. They suggested that a correlation exists between the reduction in the cross-sectional area of the psoas major (Spearmann’s rho = 0.8; P = 0.05) and the duration of continuous sciatica of the affected side but that no correlation exists between the amount of disc herniation and reduction in psoas major cross-sectional area. Similarly, Danneels et al. examined the trunk muscles (paraspinal, psoas and multifidus) in chronic low back pain patients and healthy control subjects employing computerized tomography at three different lumbar levels. These authors found no significant differences in the cross-sectional area of the psoas major or paraspinals but they did find significant differences existed in the cross-sectional area of the multifidus at the L4 spinal level. Barker et al. investigated the cross-sectional of the psoas major in the presence of unilateral low back pain through the utilization of magnetic resonance imaging (MRI). These authors found that there were statistically significant differences in cross-sectional area of the psoas major between sides (median reduction was 12.3%) at the levels of L1–L5 and that there was a positive correlation between a decreased cross-sectional area of the psoas major and the duration of symptoms.

SOMETHING TO PONDER:

Now going back to dinner, consider the souce of what is on your plate with what we just reviewed.  What type of demands are fucntional for our bovine commodities?  Stability?  Or fast twtich movement?  Perhaps, as in other parts of the body, like Gastrocnemeus, Psoas Major ends up being a product of it’s environmental demands?  Does the high level athlete dictate a different function our of psoas than the standard poplulation?  In 2009, Arbanas found that psoas had a predominance of type IIA muscle fibres, whereas type I muscle fibres had the largest cross-sectional area. Type IIX muscle fibres were present as a far smaller percentage and had the smallest cross-sectional area. Moreover, the fibre type composition of the psoas major muscle was different between levels of its origin starting from the first lumbar to the fourth lumbar vertebra. They concluded that the fibre type composition of the psoas major muscle indicated its dynamic and postural functions, which supports the fact that it is the main flexor of the hip joint (dynamic function) and stabilizer of the lumbar spine, sacroiliac and hip joints (postural function). The cranial part of the psoas major muscle has a primarily postural role, whereas the caudal part of the muscle has a dynamic role. A common model of lumbar stability shows the musculature surrounding the spinal vertebrae forming a capsule. The top of the capsule is the diaphragm, the bottom is the pelvic floor, and the wall is formed by segmentally attaching abdominal and posterior spinal musculature, specifically the transversus abdominus and the segmental fibers of lumbar multifidus. What we have reviewed is that there is growing evidence that demonstrates how these muscles coordinate their activity to stabilize the spine. For example, transversus abdominis has been shown to co-contract with: the diaphragm; the pelvic floor; and the deep fibres of lumbar multifidus. According to this model, the psoas major is ideally located to assist in a stabilizing role. Psoas major has intimate anatomical attachments to the diaphragm and the pelvic floor. This unique anatomical location allows the psoas major to act as a link between these structures and may help in maintaining the stability of the lumbar cylinder mechanism. More focus might be spent on challenging “why” the Psoas Major is tonic to protect in the first place.  Facet restrictions, changes in the SIJ, strong muscle imbalance imposing a force on the lumbar segments, sustained postures, and anatomical changes might all contribute to having the Psoas sense a “threat” to this area and act to protect what it doesn’t understand.  Not wanting to get too much into the current pain science movement during this blog, I will leave that…at that.

 

Eric M. Dinkins, PT, MS, OCS, Cert. MT, MCTA

Motion Guidance

share this blog on socials

Load and Reload: Insight into Heavy Metal's Subliminal Physio Messages

Load. Re-Load. Common principals of the physio practice. Perhaps unbeknownst to the average metal fan, Metallica’s themes are often heavily laced with physical therapy metaphor, even to the extent of album names. This blog takes a look at some basic principals of loading, as well as some tangible thoughts as to clinical implication.

First, lets look at general mechanical loading of a common treatment area in clinic: Lower Back Pain. Mechanical loading is healthy, and beneficial for a spine. Loading prompts tissue repair, regeneration, and tissue adaptation, which is why proper loading is crucial to returning injured tissue (think post total hip, patients are walking day 1) or uninjured painful tissue (insert your patient’s complaint here, post-average tissue healing time.) However, localized loading at abnormally high doses, or doses exceeding the given tissues relative tolerance, can result in a pain response in that innervated tissue. The vertebra itself, as well as disc (mostly peripheral annulus), facets and ligaments are all rich in nociceptive free nerve endings. Thus all these structures have capacity to experience pain.

A patient’s loading strategy can be altered, when the patient is in pain. Things affecting the loads on the spine can be abnormal muscle tension, guarded or aberrant motions (adaptive or mal-adaptive), the patient’s perception of the task (“I know this movement will cause pain!”), and of course the excessive “un-silenced” nociceptive inputs that the painful area has acquired. Some potentially useful things research has shown us regarding patients with back pain:

  • EMG studies have demonstrated that when normal people bend forward, their back muscles are temporarily inhibited and silent, though when patients with back pain bend forward the back extensor muscle EMG shows the muscles remain active. (Ahern et al 1988, Adams et al 2002)
  • LBP patients have reduced positional sense (or “JPE/ joint positional error as much of Dr. J. Trevelean’s research on the cervical spine after whiplash has demonstrated) possibly due to altered proprioceptive nerve function (Brumagne et al 2000).

 

However, we need to remember that when considering our patients ability to perform certain exercise or contract certain muscles (Hodges and Richardson show delayed TrA contraction in LBP patients), even if we CAN assess these minute altercations, we are assessing under the influence of pain. These aberrant findings may start as a protective response to pain (to a real, biomechanical trigger), and last as a cycle induced by sensitized tissue, without actual damage or physiological need for protection.

Once tissue is sensitized, pain thresholds are lowered (your bodies way of “monitoring” the site of initial increased input/information), and often you end up with the full package (lets call this the Pain Response Package, or PRP): quality of movement changes, muscle tension relationships change, suddenly activities that were prior oblivious to one’s stream of consciousness are suddenly approached with a flood of pessimistic and often fearful cognitive processes- which has potential to further affect behavior and experience of the given task. Suddenly Granny views a patio step as the trail of tears. The pain response package (PRP), for understandable reason, often yields a deconditioned state of the painful area, and with some, a deconditioned body.

Enter Metallica, enter the sandman, enter loading. What do we know about avoiding loads to the body (ie immobilization)? It is a catalyst to deterioration, and joints undergo physiological changes that amount to softening of cartilage, chemical changes, and structural changes for the worse (http://www.ncbi.nlm.nih.gov/pubmed/3581580).  Now, most people in pain have not become completely immobilized, but at a tissue level the collective processes that lead to poor tissue health begin. If you put your elbow in a brace for 6 weeks, is it stiff upon removal? Does your back pain patient also have stiffness? Is there tissue starting to undergo a change, for the worse?

The patients reaction to the PRP (all the things that come along with pain) IS a DYSFUNCTION- it doesn’t necessarily entail permanent damage, irreversible damage, or any real damage at all on a tissue level. I will take a moment to note that unloading has its place (think heel lift for severe Achilles tendonitis), and Metallica could have introduced a short EP titled “Unload”, which can be a necessity for your patients at times- but these times should be brief, with the anticipation of load and re-load on the horizon.

So this can simplify some things: we as physios are always looking for “the cause” and verbally manifesting (sometimes off-the-cuff) elaborate explanations of the culprit, and what needs to be “fixed”.  Our credentials can be elongated and our identities given an ego boost, in becoming “certified” in a litany of methods of assessment and treatment, which usually become the reference grounds for our explanations to patients, hopefully watered-down. But we don’t have to have an external cause for pain, and scare the patient with images of their degenerating disc. It is the present state of the patient that should be of concern (argues Waddell in “The Back Pain Revolution”, 2004). So is the dysfunction a loss of physical capacity, or a matter of performance? Waddell asks. Treatment can be effective, but research is showing its efficacy is likely “non-specific” (sound like familiar terminology from the past few decades of research in manual therapy?) The manifestation of physical dysfunction (all the things we eagerly jot down about hypertonicity, stiffness, shortness, strength and quality) are much more important than the long-deceased trigger, and can all potentially affect loading. And they are all part of the current state the patient presents themselves in. And keep in mind, the “trigger” is what the patient is sweating, as they have been ruminating thoughts of certain aforementioned “collapsing discs” and “arthritic facets” and other forebodinglingo ejected from the mouths of their trusted lab-coat donning MDs, as well as perhaps other physios and WebMD.

The BIOMECHANICS of the patient’s current pain state MATTER, though it may be a paradox: they may not matter in the sense of the “trigger”, but they matter in the “response” to the trigger. 2 points to illustrate this concept:

  • Take a patient that once suffered sciatica, and got better after 6 months: This person with discogenic radiculopathy, in raging pain at its onset, will have the SAME MRI result when they are happily sipping tea, free of all pain, 6 months later.
  • Complaints of back pain do not increase with age, but peak in mid life- thus all the biomechanical things we consider about facet compression with position and loads and tissue tolerance do NOT necessarily abide by the rules of biomechanics in relation to pain (they don’t seem to have a linear, or positive relationship, when looking at the lifespan).

So when a patient is in a state where normal afferent input = interpreted as pain, loading plays a vital role in the road to recovery. Loading is a broad term, and can be applied through simply moving, isometrics, isotonics, etc. This is where physical therapist can apply relevant information gathered from their assessment to help their patient improve. We can educate the patient with a concept as simple as “Wolff’s Law”, the theory developed by the German anatomist and surgeon Julius Wolff that states that bone in a healthy person or animal will adapt to the loads under which it is placed. Use Wolff's law as a euphemism when explaining stenosis and bone spurs: its just your bodies way of trying to increase surface area to disperse load! 

Questions to ponder:

  • Is the painful area subject to higher loads that could be temporarily avoided by changing mechanics, to allow desensitization? (can you temporarily change the way they are performing a painful task, to load different tissue, strengthen out of the familiar painful ream as to return to it at a later time when tissue tolerance increases?
  • Does their body allow options for movement strategy? If every time your patient squats they fall into the exact same pattern, do they have the strength or control to perform this task outside of that pattern?
  • What load can your patient tolerate without a “flare-up”? Can the patient conceptualize this? What we know about tissue adaptation should support this as a starting point, and encourage progressive loading in low level pain zones. Build upon this and make sure the patient is noting their loading tolerance as they improve!
  • Are there restrictions in the patient’s movement that may be causing the loading to be overly repetitive and unnecessary? Are these restrictions tissue-length based, joint-restriction based, or fear/avoidance based? What areas can we work on to change this?
  • What lifestyle loads may be contributing to sustained protective behavior? Can we alter how they are working, sitting, standing, with education that this is only a temporary need to break the cycle of protection? 

Loading can be simple, or complex, and research is still being conducted to help physios understand how particular tissues respond to particular loading.

For tendons alone, a see:

 Michener et al. J Orthop Sports Phys Ther 2015;45(11):829-832. doi:10.2519/jospt.2015.0114
 Plinsinga et al. J Orthop Sports Phys Ther 2015;45(11):864-875. Epub 21 Sep 2015. doi:10.2519/jospt.2015.5895
 Couppe et al. Journal of orthopaedic & sports physical therapy | volume 45 | number 11 | november 2015 | 853

The underlying theme however, is there is rarely a time when all forms of loading need to be avoided, and that loading does not have to be overly specific to result in decreased pain and increased function.

-Tal Blair, DPT

share this blog on socials

 

 

Another rocker's attempt at reaching physios in a some-what obvious reference to Wolff's Law.

Another rocker's attempt at reaching physios in a some-what obvious reference to Wolff's Law.

RESTING STRESS FACE (RSF)

I’m not sure the origin of this fellow but he looks a bit stressed. He is clearly alarmed, and ready to scurry off to somewhere less exposed. It doesn’t take a physiognomy-specialized psychologist to recognize that he is on high-alert. Candidate for a manip? Probably not. Heavy on the fear-avoidance scale.

Lets take a closer gander:

Yes, sympathetic juices are flowing. Heart rates up, pupils are dilated, arrector pili muslcles in full force, and a tactical exposure of the one defense mechanism this critters got going for him (sharp teeth) - a characteristic likely evolved from years of startling harassment via his predators.

So, how do you deal with a patient with “resting stress face”?  RSF.

First of all, by recognizing it. Facial features are a display of emotion, state of health, and subconscious or conscious current perceived threat level. Treatment is often dictated based on facial features and body language. A grimace says “don’t go there”, and no matter what you are trying to achieve, I doubt it will be successful if your treatments are full of grimace evoking “digs” for the soul purpose of thinking you “found the spot” (unless laced with a HEAVY dose of placebo.) Even if a pain-evoking maneuver somehow WAS necessary, do you think the patient body’s reaction would be conducive to maintaining that? The body’s reaction to what you are introducing is mediated by the patient’s perception of the interaction, and if that interaction has already began in a state of fear/stress/pain (ie sympathetic state), hopes of disengaging that via “fight fire with fire” appears an odd strategy.

Of course, there are the outliers who come in to their sessions with masochistic desire for a heavy-handed therapist to dig out the pain- and I believe expectations are well-linked to success rates. How a patient THINKS they will respond to treatment, has PREDICTIVE VALUE on how they actually respond. This has been validated in research looking at surgical outcomes, as attitudinal and mood factors were strongly predictive of surgical outcomes (Rosenberger et al 2006). You don’t have necessarily to ditch the IT-band fascia release to appease the guy (or gal) demanding it, but in my case I am left feeling like a bit of a con-man lest I use this opportunity to discuss WHY this high-stimulus blast of inputs may individually favor that person. And even that could backfire, and requires a hell of a lot of tact! Maybe dealing with that interaction is truly the art, in the art & science of PT.

Back to RSF…

RSF is probably a yellow flag.

There is research that links stress level to delayed healing. The science of that is basically that stress increases release of cortisol, which facilitates anti-inflammatory mechanisms, and decreases pro-inflammatory mechanisms, and has an inhibitory effect on the immune system (which is why persons on long-term steroids are prone to infection/disease/illness and need to be careful.) Ever wonder why everyone is sick during finals week? Stress much? Cortisol may be good in the short term, but actually delays healing! After all, the process of inflammation is one’s body sending immune cells to the site and eventually assisting in the repair phase of the tissue.  

Cortisone injections are pretty popular. I’m not against these, as they may certainly be a better option than going under the blade, and actually do physiological change the tissue environment and may open a window for change if conservative measures fail. However, I don’t think they should be first on the menu.

One research article notes: “3824 trials were identified and 41 met inclusion criteria, providing data for 2672 participants. We showed consistent findings between many high-quality randomised controlled trials that corticosteroid injections reduced pain in the short term compared with other interventions, but this effect was reversed at intermediate and long terms”(Coombs et al. 2010)

 Essentially a short-term blast of pain relief (mechanisms may include removal of neurally sensitizing agents inherent to inflammation, immediate placebo effect of getting “something done” to the tissue, and a rapid chemical change in the affected environment) is at the potential cost of a slower recovery.

Further research has been conducted regarding tissue healing in stressed-out rats (as if the rat-life isn’t stressful enough); the DIY research project would be conducted as follows: grab two of the closest rats, jab them with something sharp, let one roam freely in a fun-filled rat amusement park, ruffled by soft wood shavings, neutral colors and self-propelled exercise wheels, and put the other in a tight tube that makes all the limbs immobile and only allows breathing (we haven’t tried this on humans yet, probably a euro study in the mix…) and what do you find? The wound healed 27% slower in the stressed rats vs the non-stressed, and they showed 2.5x greater growth of staphylococcus (ie higher risk of infection) as well as higher cortisol levels. (Padgett et al 1998)

And here is a great link to a paper that looks at stress in not only mice but humans too:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3052954/#R13

Fun facts:
Students with wounds heel on average 40% slower during exams compared to being on holiday. Also, research found persons living stressful lives heal 24% (Marucha 1998) and persons in hostile environments/relationships heal up to 60% slower (Kielcolt-Glaser et al 2005).

So how do we assist in alleviating stress in our patients? I would argue for:

1) Thorough evaluation and sensible explanations

2) Listening to the patient’s FULL account of their experience and evaluating the patients’ view of their pain/issue and considering that in your explanation/delivery of your treatment plan (not to mention GIVING a treatment plan…preferably with an overall internal locus of control)

3) Considering the individual when applying a treatment (ie what matters is how they react to your treatment, and how their bodies physiologically react, which is often NOT biomechanically sensible!)

An example of a thorough evaluation of say a person with sciatica would be ruling out signs of nerve damage, and telling a patient “because your reflexes are intact, you have good sensation, and we don’t see any weakness in the muscles, this is a great indicator that you are not experiencing any true nerve damage. While I understand your problem is with pain, pain is not necessarily a good indicator of tissue damage, or even tissue health (and go on to give examples)”. Knowledge of this on behalf of the patient may alone promote stress relief.

Considering the individual’s view of their pain and applying that to your explanation is where some craft is involved. You don’t always want to go all Butler/Moseley on a patient and start launching explain-pain rhetoric, as what your scholarly view intends and what message actually gets across can be very different (not to devalue their research and their messages as they are a HUGE attribute, but I think we need to use good judgment on what verbal information is, on the patients’ side of the coin, mentally impregnable). Be simple. I went through a phase of WAY too technical explanations regarding my sometimes incoherent understandings of pain processes. If the patient is interested, and the interactions cater to it, I may use something like this:

“Your tissue is full of tiny nerves that pick up on stimulus, such as mechanical (poke on their leg lightly now) stimulus and chemical stimulus such as inflammation. Something increased the sensitivity of your tissues here, so now with 10% stimulus, the tissue reacts as if it is undergoing 80% stimulus. This causes lots of protective behavior in the tissues, like muscle tightness to control everything, and heightened pain perception so your tissue can analyze EVERY little thing that happens to it. That is just how our body sometimes deals with things, and it’s the body’s way of paying close attention to the area. What we need to do is desensitize the tissue, by SLOWLY allowing it to accommodate to an increase in stimulus, and we can do that in the following ways…”

“the following ways” is where a huge amount of freedom comes in, and although there are a million guru explanations for specific and technical applications of specialized skilled techniques, it think in reality were just desensitizing the tissue via a few somewhat explained and hopefully admittedly unexplained mechanisms. Loading tissue in novel ways can be a great way to do this, as can strengthening surrounding areas, as can reducing stress, as can giving a patient a plan. Lets leave the mechanisms of treatment for another day.

In summary, try to help your patient find ways to both understand how stress may negatively affect them, and to seek strategies to alleviate stress. Simple exercise may be the answer. Or meditation may be useful for your patients in sandals. Or maybe a glass of wine and a mental break from the days stressors. Try to promote a positive view of the condition by avoiding stressful terminology (avoid constantly referring their disc herniation, tear or “blocked segment”.) Be aware of your patients’ view of their problem, and attempt to be a good judge of their level of acceptance to your treatment, using verbal, visual, and tactile cues to fill in the gaps when beneficial. 

-Tal Blair, DPT

share this blog on socials

Youth ACL Injuries: Preventable?

Youth ACL injuries appear to be on the rise. Adult ACL injuries have been the hot topic in decades of research in an attempt to reduce the frequency of these injuries, especially in sports.  But why the recent increase in ACL injuries in kids?  According to Moksnes et al 2013, most ACL tears come fromAlpine skiing and soccer making up 73% of injuries in that study.  As this was an international study, American football wasn’t available for the population to study. Mix this finding with results of a Mansson et al AJSM 2014 study who found that the cause of injury was 55% contact and only 21% non-contact.  Almost the exact opposite of mechanism in adult injury:

So are we setting up our children for life changing injury based on the sports they chose (or we chose for them)?

In the long term, patients who were adolescents at the time of their ACL reconstruction revealed significantly more radiographically visible OA changes in their operated knee than in the non-op knee. Rarnski et al 2013 investigated Anterior Cruciate Ligament tears in children and adolescents and found in their Meta-analysis 13.6% of reconstructed felt instability compared to 75% of non-operative and meniscal tears were 12x more likely in non-op group (35.4 vs 3.9%). 

Anderson and Anderson 2014 AJSM stated that the independent risk factors for incidence of lateral meniscal tears were younger age and return to sports prior to surgery.  Subjects with one (1) incident of instability had a 3-fold higher odd of a high grade lateral meniscal tear.  And chondral injury factors were instability episodes and increased time to surgery. Subjects with meniscal injuries were more likely to have chondral injures in the same compartment. Preservation of the menisci may theoretically reduce the changes of articular cartilage degeneration and the additional risk of OA.

However, there have been studies that have found that the prevalence of meniscus injuries at only 29% at 3.8 year follow up and 88% reported returning to monthly cutting and pivoting tasks at school.  It should be of strong note that those individuals who were non-operative were instructed in a treatment algorithm and 1/3 changed their activity at F/U. Somewhat deceptive to the reader of only the abstract.

 

Surgical Reconstruction Options

 

From a surgical standpoint, social, psychological, demographic and age dependent factors all need to be considered in every case.  And currently there is no consensus in literature about transphyseal ACL recon, physeal sparing, or non-op. Although likely that physeal sparing early reconstruction is probably better in terms of incidence of menisci and chondral injury compared to delayed.  The return to sport and decline in participation is obvious and substantial 2-3 years non-operatively in most research studies on this topic.

According to a 2013 study, children and adolescents who undergo early surgical reconstruction after suffering a complete tear of the anterior cruciate ligament (ACL) have much better outcomes than those who delay surgery or never have surgery at all.

Reviewing data from six studies comparing operative to nonoperative treatment and five studies comparing early to delayed reconstruction, researchers at the Children's Hospital of Philadelphia found that patients in the nonoperative or delayed group were 33 times more likely to have persistent instability in the injured knee than those whose ACL tears were treated surgically.  

In terms of return to play, athletes who had early ACL reconstruction were 91.2-times more likely to return to activity at the athlete's previous level of play than those who did not have surgery, who were also much more likely (67% versus 4%) to subsequently suffer a tear of the medial meniscus. “Our results suggest that patients are much more likely to return to sports at their previous level of athletic ability after early operative treatment as well as have fewer instances of instability" of the knee or meniscus tears, writes lead author, David E. Ramski, BS, BM, of the Georgetown University School of Medicine.  

 

 

In terms of return to play, athletes who had early ACL reconstruction were 91.2-times more likely to return to activity at the athlete's previous level of play than those who did not have surgery, who were also much more likely (67% versus 4%) to subsequently suffer a tear of the medial meniscus. “Our results suggest that patients are much more likely to return to sports at their previous level of athletic ability after early operative treatment as well as have fewer instances of instability" of the knee or meniscus tears, writes lead author, David E. Ramski, BS, BM, of the Georgetown University School of Medicine.

The decision making challenge after ACL injuries in the pediatric patient presents itself for surgeons and young athletes as a dichotomy between protecting a developing growth plate and preserving the integrity of the meniscus.

But potential risks to the growth plate with ACL reconstruction must be balanced by the risks of potential damage to the medial meniscus and chondral damage in patients treated with non-operative measures. 

bone.png

The availability of surgical techniques that spare or avoid the growth plates when reconstructing the ACL in skeletally immature patients, and limited evidence that surgery arrests the growth of such plates, may assuage some of the concern related to premature growth arrest or deformity with early reconstruction, the current studies conclude that the data favor early ACL reconstruction, particularly for active young athletes who wish to maintain higher levels of physical activity.  

Based on concerns that surgery might damage growth plates at the end of the tibia and fibia in such skeletally immature patients, the optimal initial treatment for ACL injuries in children and adolescents has not resulted in a clear consensus for initial nonoperative treatment or operative reconstruction. Whether a study will lead to the development of a consensus that early ACL reconstruction is the optimal treatment remains to be seen. 

Parents should understand that early reconstruction of the ACL, before any other damage to the knee, gives their child the best chance of a good outcome in the future. Once other structures in the knee are damaged, the final outcome may not be as good, no matter what the surgeon does at the time of reconstruction. 

Some of the difficulty with non-oping kids is the ability to control their activity.  Telling children to simply stop moving a certain way is a near impossible challenge. Most current research studies strongly imply that delaying ACL surgery and reconstruction puts an athletically or even a normally active teenager at significant risk for re-injury, and for injury to other structures in the knee.  

 

As detailed in a recent study in the Journal of Bone and Joint Surgery the indirect costs (e.g. lost wages, productivity, and disability) associated with an unstable knee after an ACL tear are substantial. Researchers at KNG Health Consulting in Rockville MD found that ACL reconstruction was less costly (a cost reduction of $4,503) and more effective in terms of quality of life compared with rehabilitation because of the higher probability of an unstable knee associated with rehabilitation.  

In the long term, the mean lifetime cost to society for a typical patient undergoing ACL reconstruction was less than half that for rehabilitation ($38,121 versus $88,538).  

The finding demonstrated that access to ACL reconstruction is critical to optimal societal health-care delivery.

 

So what choices do we have as rehabilitations professionals for youth clients with ACL injuries? Unfortunately, surgical medicine continues to prove that what we surgically correct now, might not be our best option, or even what we should have done a decade later in hindsight. But surgical medicine also continues to advance almost annually. Preservation of the cartilage structures should lead to the most optimal outcome in the long term and reconstructing the ACL as soon as possible appears to appeal to common sense from a biomechanical model stance. In my biased opinion, prevention must be the first line of defense.  But according Mansson, youth injuries at much more likely to be from contact than non.  Specific functional activity training can’t control all of that.  Proper coaching and conditioning might aide the cause. Cessation is an option as well.  But pulling kids from sports to avoid getting hurt is not an option many parents or coaches will likely consider.  After all, we are all superman until we get hurt…. Or as Iron Mike Tyson would say “Everyone has a plan until they get hit.”

 

This leaves this with a real dilemma for this injury in this population. 

 

Hopefully we find some answers soon. 

 

 

Eric M. Dinkins, PT, MS, OCS, Cert MT, MCTA, CCI

Motion Guidance

share this blog on socials