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Author’s Note: This is the second installment in an ongoing series on my blog, Integrative Human Performance, meant to introduce the Postural Restoration Institute and the concepts that it teaches, as well as how we integrate them into training and rehab.  You can view this post in its original format on the blog by clicking here.  If you missed the first installment, you can click here to give that a read in its original format, or click here to read it on the PRI website. In this installment, I’ll take the neurological underpinnings of PRI’s methodology (discussed in Part 1) a bit farther to discuss the biochemical and physiological responses to the different autonomic states. I’ll give a brief insight into the relevance of these responses to muscle activity at the end, and will focus in detail on how that impacts postural and movement patterns in the next couple of installments.

In the last installment, I explained that while on the surface PRI may seem solely concerned with postural and movement dysfunctions, its ultimate goal is to assess a person’s autonomic state and their relative balance of sympathetic and parasympathetic output, as well as the ability to change which division is more dominant in the face of various stimuli.  In this post, I will outline the specific physiological responses that these autonomic subdivisions elicit and detail the mechanisms by which they work.  It is my hope that this explanation will give you a better understanding of how the neurological influences outlined in part one translate to patterns of movement and muscle activity that I will describe in parts three and beyond.

Autonomic Nervous System Function: Mechanisms Responsible for its Effects

As I briefly mentioned in part one, higher brain centers in the limbic system and even the cerebral cortex send information to peripheral effectors via action potentials through efferent neuronal circuits.  These circuits pass through the brainstem, which contains the reticular formation in the pons and medulla.  While in the first post I described how these nerve impulses can impact muscle tone and activity, I only briefly mentioned that they also impact traditional “autonomic functions” such as heart rate and the rate and depth of ventilation.  In fact, the input the brainstem has in cardiorespiratory function is, at least in the sense of direct influence, more profound than its influence on skeletal muscle.  This is made apparent by the fact that the Cardiovascular Control Center (CCC) and the Respiratory Control Center (RCC), which are responsible for regulation of heart and breathing activity, respectively, are both located in the brainstem.

The Cardiovascular Control Center is in the medulla oblongata (cue the obligatory The Waterboyreference). The CCC innervates the heart with parasympathetic fibers via the vagus nerve (which I mentioned briefly in part one) as well as via sympathetic cardiac accelerator nerves.  While cardiomyocytes can spontaneously depolarize and initiate a heartbeat, these autonomic nerves enable the CCC to alter heart function in response to afferent feedback from peripheral chemoreceptors and mechanoreceptors as well as efferent feedforward stimulation via higher brain centers.  At rest, the parasympathetic system predominates and allows for relatively minor changes in heart activity by increasing or decreasing its output.  In other words, the sympathetic system does not appreciably contribute to adjustments to cardiac activity at rest.  The same is actually true of the onset of exercise–the increase in heart rate and contraction force are largely due to the withdrawal of parasympathetic output up to approximately 100 beats per minute, at which point the sympathetic nervous system will increase activity to meet any further increase in demand.

The Respiratory Control Center is also located in the medulla oblongata as well as in the pons.  The most widely-accepted theory behind its function is the Group Pacemaker Hypothesis, which states that there are four distinct regions that are responsible for initiating and regulating the breathing process, two in each of the aforementioned subdivisions of the brainstem.  The Dorsal Respiratory Group (DRG), located in the medulla oblongata, is generally considered to be responsible for initiation of inspiration at rest.  Cells in the Solitary Tract Nucleus propagate signals to the Retrotrapezoid Nucleus, which in turn innervates respiratory muscles like the diaphragm and the external intercostals via the phrenic and intercostal nerves, respectively.  The Ventral Respiratory Group (VRG, also in the medulla oblongata), on the other hand, acts secondarily to the DRG and is generally thought to be active only during forced breathing, like when you exercise.  There is still some debate over this latter point, however, since the preBotzinger Complex, which is located in the Ventral Respiratory Group, has been hypothesized to be the structure primarily responsible for the initiation of spontaneous breathing as well as the generation of the rhythmic pattern of ventilation.  The two other regions involved in the breathing process, the Apneustic Center and the Pneumotaxic Center, are located in the pons.  The Apneustic Centers (there is one on each side of the brainstem) regulate inspiration by influencing the DRG.  Continuous firing of the Apneustic Centers stimulates the DRG, consequently increasing the depth and rate of inhalation.  The Pneumotaxic Centers (also one on each side of the brainstem), in contrast, are innervated by the Vagus Nerve, and upon stimulation inhibit the Apneustic Centers, thus promoting exhalation.  Much like the CCC, the RCC can respond to input from both peripheral chemoreceptors as well as higher brain centers.  It appears that input from higher Central Nervous System structures, such as the hypothalamus and cerebrum, to the Pneumotaxic Centers provides the primary drive for initiation of the respiration cycle, while peripheral sensory feedback fine-tunes the regulation process.  It is possible, however, for normal respiratory cycles to continue in the absence of input from higher brain centers, so long as the damage is done above the level of the pons.  This phenomena is called redundant control, and is a mechanism that increases the likelihood of survival of the organism since multiple systems must fail in order for function to be lost.

One point to highlight with regards to the Respiratory Control Center is that its innervation of the respiratory muscles is via somatic motor neurons, which are not traditionally classified as autonomic in nature despite the fact that those innervating respiratory muscles are largely under involuntary control.  This does not mean, however, that the Autonomic Nervous System has no influence on respiration.  When subcortical structures in the limbic system are activated in response to a perceived threat, it is believed that they can bypass the respiratory centers altogether via extrapyramidal upper motor neuron fibers that innervate the same lower motor neurons that are controlled by the DRG and VRG and are responsible for respiratory muscle activity.  In addition, higher centers can also exert inhibitory effects on the Apneustic and Pneumotaxic Centers.  The inhibition of the Apneustic Centers is apparent when you try to hold your breath as long as you can, since the Vagus Nerve (specifically the Ventral Vagal Complex, or VVC) stimulates the Pneumotaxic Centers, which inhibit the Apneustic Centers.  The result is a suppression of inhalation, although this ability is obviously limited, as evidenced by the fact that you can’t kill yourself by simply holding your breath–you are forced to inhale eventually. (Author’s Note: even though we’re quite confident in this claim, for liability reasons we recommend you don’t test it at home.) Inhibition of the Pneumotaxic Centers, on the other hand, is a result of decreased Ventral Vagal Complex tone and causes an inhibition (or rather a lack of excitation) of the Pneumotaxic Centers.  This, in turn, impairs the Pneumotaxic Centers’ ability to inhibit the Apneustic Centers, which become hyperactive and facilitate an increase in the length and depth of inspiration.  Recall that I mentioned the VVC and its effect on the balance of sympathetic and parasympathetic function in part one of this series.  Be sure to make note of the facilitation of inspiration when the parasympathetic activity of the VVC is diminished, since that will resurface later in this post and in subsequent installments.

The takeaway here is that in addition to potential direct and indirect influences on skeletal muscle, the autonomic nervous system has a profound direct influence over basic autonomic functions such as cardiac and ventilatory activity.  Both the cardiac and respiratory control centers in the brainstem can respond to feedback from peripheral sensory receptors as well as descending input from higher brain centers in anticipation of a threat.  Parasympathetic input to the heart predominates at rest, while a withdrawal of parasympathetic outflow and subsequent increase in sympathetic outflow causes an increase in heart rate and force of contraction.  Parasympathetic input to the respiratory control centers is characterized by an increase in ventral vagal tone, which leads to an increase in the length and depth of expiration secondary to a decrease in the length and depth of inspiration.  Sympathetic input to the respiratory control center is characterized by a decrease in ventral vagal tone, which leads to subsequent increase in the length and depth of inspiration and concomitant decrease in the length and depth of expiration.

Sympathetic Nervous System Activation: The Response to Subcortical Threat Appraisal

In the previous section I established that the autonomic nervous system has considerable control over the function of both the heart and the respiratory muscles.  What I specifically want to examine now is the response that the autonomic nervous system has to perceived threats, and the effect that that response has on cardiorespiratory functions.

Structures of the limbic system (e.g. the amygdala and cingulate gyrus) and some higher centers (e.g. the insula) are responsible for initiating emotional responses and regulating threat appraisal.  When a threat is perceived, multiple responses can be undertaken due to the evolution of the Vagus Nerve in mammals, as explained by Stephen Porges’ Polyvagal Theory.  The most evolutionarily recent response, which correlates with the more evolutionarily recent ventral portion of the Vagus Nerve, is the suppression of sympathetic activity by the Ventral Vagal Complex in favor of prosocial behaviors such as communication and self-calming.  This response is generally the first response in humans, since it is faster due to myelination of the ventral portion of the vagal nerve.  According to the Polyvagal Theory, however, as the threat level increases or persists despite the aforementioned attempts to mitigate it via prosocial behaviors, we tend to decrease ventral vagal tone and “fall back” on more primitive responses.  One such response is the fight-or-flight response, which can occur when the VVC fails to inhibit or attenuate sympathetic output.   As sympathetic output increases, we see a number of physiological effects.

With regards to the autonomic functions discussed previously, cardiorespiratory activity will increase with increased sympathetic outflow.  The cardiac accelerator nerves to the heart will increase their rate of firing and release the catecholamine norepinephrine at the sinoatrial node and ventricles of the heart.  This neurotransmitter activates beta-1 adrenergic receptors in these regions of the heart, which activate G proteins in the cytoplasmic leaflet of the cell membrane.  G proteins in turn activate cyclic AMP (cAMP), an intracellular second messenger molecule that is responsible for activating cellular enzymes like protein kinase A that will, in the case of cardiomyocytes, increase heart rate and force of contraction.  In addition, sympathetic input to the adrenal medulla causes the release of the catecholamine epinephrine  (and to a lesser extent, norepinephrine) into the blood.  Epinephrine (and to a lesser extent, norepinephrine) activates alpha-1 adrenergic receptors in smooth muscle cells lining blood vessels, again activating a G protein in the cytoplasmic leaflet of the cell membrane.  This G protein, in contrast to those associated with beta-2 adrenergic receptors, binds to a membrane-associated enzyme called phopholipase C.  This enzyme cleaves a phospholipid in the cell membrane called phosphatidylinositol into (1) inositol triphosphate, an intracellular signaling molecule that causes calcium ion release from the sarcoplasmic reticulum and thus contraction of the smooth muscle, and (2) diacylglycerol, another intracellular second messenger that is responsible for activating protein kinase C and the subsequent pathways it controls.  The overall result is vasoconstriction of the blood vessels.  In the vasculature that supplies active skeletal muscles, however, alpha-1 adrenergic receptors are inhibited, allowing epinephrine to activate beta-2 adrenergic receptors that promote relaxation of the smooth muscle and vasodilation of blood vessels via the aforementioned cAMP-protein kinase A pathway.  The net result is a reduction of blood flow to inactive skeletal muscles and most visceral organs and an increase in blood flow to active skeletal muscles, hepatocytes, and coronary vasculature to meet the increased metabolic demand that is either present in these cells or that the brain anticipates will be present due to the perception of an immediate threat.

As far as respiration is concerned, as I previously stated subcortical structures of the limbic system can bypass the respiratory centers in the brainstem altogether in the face of a perceived threat via extrapyramidal upper motor neuron fibers that innervate the lower motor neurons responsible for respiratory muscle activity.  An increase in the firing rate of these lower motor neurons leads to an increase in ventilation rate.  In addition, it is important to note that heart and ventilatory function are tied very closely.  Inspiratory activity is related to an increase in heart rate, primarily via a decrease in the rate of time spent in diastole (the phase of relaxation in the cardiac cycle), since the increase in the volume of the thoracic cavity with contraction and depression of the diaphragm decreases the pressure in the cavity.  The heart must respond to the lowered pressure by increasing heart rate to adequately fill the lung vasculature as well as prevent a drop in arterial pressure in the systemic vasculature, since a large quantity of blood is tied up in the pulmonary circuit during inhalation in order to facilitate oxygenation of red blood cells.  Expiration, on the other hand, is related to a decrease in heart rate due to a decrease in the volume of the thoracic cavity when the diaphragm relaxes and ascends and subsequent increase in pressure in the cavity.  The heart responds to the pressure increase by slowing heart rate to limit venous return to the lungs and to prevent an excessive increase in arterial pressure as the large quantity of blood that was just oxygenated leaves the pulmonary circuit and enters the systemic circuit.  Also recall that an increase in sympathetic activity secondary to inhibition of the ventral vagal complex causes an inhibition (or rather a lack of excitation) of the Pneumotaxic Centers in the Respiratory Control Center. This, in turn, impairs the Pneumotaxic Centers’ ability to inhibit the Apneustic Centers, which become hyperactive and facilitate an increase in the length and depth of inspiration.  Relating this to the previously outlined link between heart and ventilatory functions, the increase in heart rate caused by direct sympathetic innervation to the heart is reinforced by increased inspiratory activity caused by decreased ventral vagal tone and inhibition of the Pneumotaxic Centers of the Respiratory Control Center; this is another example of redundant control.

The takeaway is that humans, in addition to other mammals, have the unique ability to respond to a perceived threat by inhibition of sympathetic outflow via the ventral portion of the vagus nerve.  In the face of chronic or a high level of stress, however, ventral vagal tone can decrease and we can regress to the more primal response of increasing sympathetic nervous system activation, i.e. initiate the fight-or-flight response.  In this case, greater sympathetic outflow to the heart will increase its rate and force of contraction, while increases in epinephrine and norepinephrine circulating in the blood will lead to a decrease in blood flow to non-active skeletal muscle and most visceral organs and an increase in blood flow to active skeletal muscle, the liver, and the heart.  Increased firing rate of pathways connecting the limbic system to the motor neurons controlling respiratory muscles causes an increase in overall ventilation rate, while sympathetic input to the respiratory control center secondary to a decrease in ventral vagal tone causes an increase in the depth and length of inspiration and a relative decrease in the depth of length of expiration.

Sympathetic Nervous System Activation: Downstream Effects on Skeletal Muscle 

In the first installment, I described potential direct and indirect mechanisms by which the sympathetic nervous system can potentially influence resting muscle tone via gamma motor neurons innervating muscle spindles and beta-adrenergic receptors that interact with the neuromuscular junction and the sarcoplasmic reticulum.  Earlier in this article, I also described how an increase in sympathetic outflow leads to increased blood flow to active skeletal muscles, decreased blood flow to inactive skeletal muscles, and an increase in the activity of respiratory muscles.  There is one other downstream effect of sympathetic nervous system stimulation on skeletal muscle that I’d like to introduce, and it once again relates to the cardiorespiratory system.  While the ratio of inhalation to exhalation length and depth increases with sympathetic activation, the overall increase in ventilatory rate allows for increased clearance of carbon dioxide, which is a byproduct of cellular metabolism that is produced in greater amounts when metabolic activity in tissues is high.  As you can imagine, this is beneficial during times of exercise or fighting off/fleeing from a threat where metabolic demand of skeletal muscle, liver, and heart tissues will be very high, and thus CO2 accumulation will warrant its clearance.

A problem may arise, however, when sympathetic activation stimulates an increase in ventilatory activity in the absence of significantly increased metabolic demand, as could be the case when the VVC chronically fails to inhibit sympathetic outflow and we become engrained in a sympathetic-dominant state.  This system rigidity and inability to vary autonomic states may still facilitate the clearance of CO2, even if it’s not appreciably accumulating in tissues.  When blood CO2 levels fall even in minuscule amounts, blood pH rises (i.e. it becomes less acidic) and shifts the saturation curve of oxyhemoglobin to the left, a phenomena called the Bohr Effect.  This means that oxyhemoglobin, which is responsible for transporting oxygen to tissues, will have a higher affinity for oxygen at any given partial pressure of oxygen in the bloodstream.  This, in turn, impairs oxyhemoglobin’s ability to unload oxygen to the tissues, including to myoglobin in muscle tissue.  Oxidative metabolism in muscle tissue subsequently suffers, forcing the cells in these tissues to rely heavily on non-oxidative (i.e. anaerobic) metabolism.  Non-oxidative metabolism is insufficient in producing enough ATP for muscle contraction in the long-term, since oxidative metabolism is far more efficient in terms of ATP production.  Lack of ATP renders actin-myosin cross bridges that have formed unable to dissociate, a phenomena that also occurs to an obviously far greater extent in rigor mortis.  The result is a relatively rigid, shortened muscle.  Theoretically, the muscles that would be most affected by this decrease in oxyhemoglobin unloading and subsequent tissue oxygenation would be those  receiving the greatest amount of blood flow due to sympathetic-mediated vasodilation of their blood vessels, which would also be the muscles with the highest metabolic demand and work rate.  Remember that point, since it will resurface in the next couple of installments when I delve into specific patterns of muscle activity and movement.  Also of note is that anaerobic metabolism is inefficient in producing CO2 as a byproduct in comparison to oxidative metabolism.  Thus, a shift from predominately oxidative to anaerobic metabolism via chronic elevated sympathetic tone could have the effect of producing a self-sustaining or even positive feedback loop.

The takeaway here is, as I emphasized in part one, an increase in sympathetic outflow is not inherently bad, but it can cause problems when we are unable to shift out of it and into a more parasympathetic-dominant state. With regards to cardiorespiratory function, increased carbon dioxide clearance due to an increase in ventilation rate during short-term sympathetic activation is absolutely beneficial in ridding the tissues of CO2 that accumulates as a byproduct of metabolic activity.  In the long-term, however, increased clearance of CO2 in the absence of increased metabolic demand can lead to decreased oxygenation of tissues, including skeletal muscle.  The resulting shift in the affected cells from predominately oxidative to glycolytic activity may eventually impair ATP production, which, in the case of skeletal muscle, limits the release of actin-myosin cross bridges.  The net result is that the muscle becomes relatively rigid and shortened.  The muscles most affected by this mechanism are those which receive the greatest blood supply, i.e. the muscles that are doing the most work.

  

Wrapping Up

I know I threw quite a bit at you in this post, so I’m going to stop there for both your sake and mine.  I hope that this post allows you to understand the link between the neurological underpinnings of PRI outlined in the first installment and the biochemical and physiological processes by which these neurological mechanisms affect skeletal muscle.  The next post, in turn, will serve to connect these biochemical and physiological processes to the “big picture” of muscle activity, postural compensations, and movement patterns that PRI emphasizes.

References

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Hello triplanar thinkers!

For those wondering, the picture is relevant because it shows a technique not often considered for the condition treated:  keeping a severed hand alive by grafting it to the patient’s ankle, then later replanting the hand back on his arm. 

The conclusion of my story about Don didn’t involve any external fixators, but the treatment that he needed might surprise some of you.  To review, Don was the patient with left shoulder bicipital tendinosis whom I treated in part I (link) with the “gold standard” conservative orthopedic approach and part II (link) with the according postoperative approach as a good therapist has been trained to.  As mentioned, I outline this case to review the path that is so very accepted and yet, in my experience since I began training with PRI, not the most effective.  Don’s story concludes below:

Don returned to clinic 8 months after discharge with a new diagnosis of left shoulder pain with the remarks on the script “MRI negative” and “eval and treat.”  This is generally understood as physician lingo for “I have no idea what to do now…good luck with all that.” 

Upon evaluation, Don reported that these left shoulder symptoms started about 2-3 months after we discharged him from PT intervention in spite of his persistence with his HEP and “it was all back to the starting point three months later.”  He still tested as a bilateral brachial chain patient with a PEC pattern, again was positive with impingement tests—Hawkins-kennedy, empty can, Neer sign.  He was frustrated, unable to work in his wood shop or play his accordion for more than 10 minutes without severe pain.  At this point, the patient and I discussed that fact that I had let him down to a degree because I wanted to take a different approach before surgery, but didn’t want to irritate Don or his referral source.  He understood, accepted my apology and we moved forward.

During the first 3 visits, we established that his bilateral brachial chain pattern and according left shoulder dysfunction was not the root of his dysfunction, but rather the manifestation of a “bottom up” pelvis patient whose primary difficulty was in maintaining frontal plane position of his pelvis. 

The key to Don’s left shoulder function?  Right posterior inlet inhibition of his pelvis.  During the seven visits we treated Don using a PRI approach after the gold standard of orthopedic medicine and orthopedic physical therapy had failed to maintain his shoulder function for more than 3 months, his symptoms resolved.  He left the clinic a reciprocal, alternating, smiling woodshop athlete with bilateral HADLT tests of 4/5 at 72 years of age, “tickled” that he could play his accordion as long as he wanted without pain for the first time since before he first went to see the doctor more than two years prior.  Don is in occasional contact for the past 6 months with no return of symptoms, lots of activity and happy thoughts. 

Six-month follow-up with no return of symptoms after the rest of my conservative clinical skills, an appropriate surgery and present day gold-standard postoperative care was unsuccessful.  These are the types of outcomes that keep my passion for this science alive and accelerating.  Moreover, these are the types of patient successes that remind me to be gentle but bold about intervention that I know clinically to be the most effective tool I have in the entire tool chest.

Clearly, each patient is different, and no, I have not seen a consistent correlation over time between the diagnosis of left shoulder bicipital tendinosis and the need for right posterior inlet inhibition.  The objective tests guided me to find the appropriate treatment, not my innate ability to hear the pelvis or shoulder speak to me. 

The point here is not to create a case study for anyone to memorize to use in the future for that one seemingly random patient.  Rather, I hope that the take home is that there is a chance that this gentleman didn’t need as much intervention as he ended up having.  And, even in the face of the “old school” telling you exactly what they want from PT intervention, the risk is worth the reward if one can just take the first three or four visits to break down barriers to a different way of approaching an age-old mechanical dysfunction of a “shoulder.”

Thank you for reading, perhaps you can save a few visits for a few of your patients by way of my experience with Don.   My best to you!

Jess

I have the benefit of being associated with some outstanding thinkers and PRI practitioners.  Whenever and wherever we get together, conversation eventually drifts toward discussion of PRI principles and application.  One of our greatest challenges has been to unravel the foundations from which Ron Hruska evolved the Postural Restoration Institute system of evaluation and treatment that we all utilize with such great success. 

The following are just a couple of questions that we have posed and our attempts to reach conclusions and greater understanding.  If anything it may stimulate some thought and initiate some discussion.

What are we actually measuring when we place a patient on the treatment table and perform our PRI testing algorithm and what is our goal for treatment?

I clearly recall a conversation over lunch between Eric Oetter, Mike Robertson, and myself during the PRI Pelvis Restoration course at the Cantrell Center for Physical Therapy and Wellness. We were discussing the concepts of adaptive capacity, adaptive potential, movement variability, what we are actually measuring when evaluating a patient on the treatment table, and how this affects performance.  

Our conclusion was that what we are actually measuring as PRI-educated therapists and coaches is the capacity of our client/athlete to adapt to the ever chaotic nature of the environment they are perceiving.  Positive findings during examination such as a positive Adduction Drop Test, limited apical expansion, or loss of shoulder rotation was merely indicative of a human system incapable of demonstrating variability ultimately controlled by the central nervous system.  More specifically an autonomic nervous system shift toward sympathetic dominance.

I was reminded of this PRI lunch after reading a blog post recently that referenced the following study:

http://www.ncbi.nlm.nih.gov/pubmed/24502841

In essence, what the researchers found in the study was that pain-free subjects demonstrated variability in the muscle activity of the erector spinae during a repetitive lifting task and those with low back pain did not demonstrate this variability as well as experiencing increased pain during the task.

The authors’ conclusion was that reduced variability of muscle activity may have important implications for the provocation and recurrence of LBP due to repetitive tasks.

Needless to say, this study is somewhat validating for our discussion group of PRI faithful.

Truth be told, after searching there are many studies that support our lunchtime conclusion; and movement variability as a favorable concept in human function is not a new concept having its foundations in dynamic systems theory. 

From Shumway-Cook and Woollacott’s Motor Control:  Translating Research into Clinical Practice:

“… in dynamic systems theory, variability is not considered to be the result of error, but rather as a necessary condition of optimal function.  Optimal variability provides for flexible, adaptive strategies, allowing adjustment to environmental change, and as such is a central feature of normal movement.”

What the PRI model provides is a non-invasive real-time measurement of system variability determined by autonomic nervous system tone.  While EEG, heart rate variability, or galvanic skin response may be preferred methods to determine autonomic tone, these are not tools commonly used by a practicing physical therapist in a clinical setting or a coach in the training room nor would they be practical. 

The goal of treatment then becomes restoring an optimal level of variability to the system to allow for optimization of behavior and maximization of performance.

We came up with a statement that encompassed our entire discussion that included the influence of variability on pain and performance.  I still have the notes on my iPhone dated 8/24/13: 

“Restoring variability to the human system is the ultimate goal to promote neuroplastic change creating a relatively permanent change in behavior that provides adaptability within the system to cope with variability in the environment.”

In PRI terms, our goal is help a patient achieve neutral (restore variability) and then recruit the appropriate PRI planar families (neuroplastic change to remap the three planes in the brain… Thanks to Zac Cupples!) to restore reciprocal and alternating movement (change behavior to cope with the environment).

How did Ron Hruska arrive at the concept of using simple, common orthopedic tests as effective PRI measurement tools?

As mentioned above, as physical therapists our measurement tools are limited by practicality.  If we look at PRI from a strictly biomechanical perspective, the PRI methodology provides for a low barrier of entry to a PT who has never been exposed to its concepts before.  Myokinematic Restoration looks, sounds, and feels like biomechanical course, but we all know that it is not.  This is a brilliant way to provide understanding to a group with more than a few preconceived notions, right?

While I certainly cannot speak for Ron, and I’m willing to be wrong, I believe there is more to this process, and this came from a conversation I had with Eric Oetter over Sunday breakfast.

From our first day in an introductory PRI course we are shown that asymmetry because of in-utero development and positioning, brain hemispheric dominance, asymmetrical vestibular development, and internal anatomical differences is normal, expected, and predictable.  Determining patterning that represents discord in the system then seems to be impossible until your realize that the skeletal system, is inherently symmetrical.  Therefore there is no better way for a physical therapist to determine the state of the system as a whole than identifying asymmetries or patterns via our typical orthopedic testing.

The brain processes and integrates all sensory inputs, internal and external, and generates behavior, including motor behavior, based on our perceptions with respect to the environment, emotional status, and previous experiences.  I don’t think it’s unreasonable to consider that the ability to produce reciprocal and alternating movement is not only an effective measure of autonomic tone but also a key measurement of overall health.

Bill Hartman, PT

“Its Monday Morning, I’ve just taken my first PRI course and now what do I do and where do I start?”

If you have just taken your first PRI course and you feel a bit overloaded with information, don’t feel alone.  The first time I went to a PRI course, can I tell you I was intrigued, stunned and just a bit intimidated all at the same time?  I didn’t know what the heck I was doing so on Monday morning I had a bunch of people blowing up balloons! (Take the Postural Respiration course and you will know what I mean!)

In fact, the entire body of knowledge of PRI can feel like one big elephant you are trying to digest.  And you know the old question, how do you eat an elephant?  One bite at a time!

The first thing to do is what you learn in every course and that is to breathe and relax. There is a lot information here that needs to sink in over time and you won’t get it all the first time. No one that has taken one of these courses has gotten it all the first time but if a door is opened to your curiosity and caring to learn more you are definitely on the right track!

What helped me in my overwhelm was to create a picture in my mind of some of the basics.  For instance, we aren’t symmetrical and never will be but the point is to manage asymmetries and get neutral. Then, have a simple picture anatomically of the basic asymmetries left and right side and how they affect position and posture thru polyarticular chains.  Remember how the diaphragm is the key player and you have a simple way to describe what you are doing to yourself, patients or clients.  They will be impressed by just a short, and I mean short, description of their anatomy and how it affects them.

On Monday morning, pick one person you feel comfortable with to experiment on.  If you have a colleague that has gone to a course practice with them.   Tell your patient that you just got out of a course and you want to try some powerful tools with them.    If you took a Myokinematics course, practice an abduction drop test and show them one basic exercise.  It is best that you practice that exercise yourself and continue to practice PRI tests and exercises yourself, so you know what it feels like and what to feel when you are in position for facilitation and inhibition.  PRI works best when we are managing our own asymmetries!

Immediately you have knowledge and application of assessment and corrective positioning that is really sophisticated and you have just scratched the surface.  You can build on this by learning a new assessment or two with a new corrective position every day.

Have your manual close.  Refer to it, study it and get a more detailed picture in your mind of how the human body works and how you can be more effective.  This is called building a body of knowledge and it doesn’t happen overnight but you can get results and get excited with just the basics and build on top of them.

If you went to a live seminar, order the home study course and review it a few times.  If you got a home course, go to a live course to interact with the instructor and fellow students.  Pack a bunch of questions in your bag when you go!  If you get a little frustrated with all the information and it doesn’t make sense all at once, then you are a normal human being!  Hang in there.  The good news is that becoming more skilled and competent is satisfying and meaningful and that building a body of knowledge and expanding what you know is just plain fun!   

To summarize part I for those who didn’t see it, I treated a gentleman with biceps tendinosis giving my best efforts to treat within the realm of what the patient and his physician expected.  He was pleased, reported 90% improvement and had met all but one of his functional goals—and I wasn’t content.  I wasn’t content because I hadn’t been bold/confident enough to risk the referral source by advocating for the patient like I had wanted to.  When things had a hitch, I had broached the subject of asymmetry several times, with a discussion of thorax and diaphragm position combined with respiration being key to arthrokinematics and myokinematics of the affected left shoulder briefly.  But the feedback each time was something of the “dang kids and their wide-eyed plans.”  So, I deferred to the ‘gold standard’ treatment of the day for said diagnosis outlined briefly in part I of this story with some PRI principles intertwined the best I could without the patient’s objection.

Three months later, Don arrived for this second round of PT with a diagnosis of left shoulder s/p arthroscopic subacromial decompression with a distal clavicle resection and biceps tenotomy.  His orders were specific to “ROM and strengthening” and he had a firm grip on what he wished to achieve per his physician’s orders.  Though I mentioned that, after the first couple of weeks, it would be wise to treat the cause rather than the symptoms of his left shoulder problem, he only agreed we’d reassess after a few weeks.

I saw him once a week for three weeks and he attained full ROM, felt wondersplendiferous (there is a small reward for whoever first tweets the three root words for this nonsensical term) and he was touting my praises loudly when he arrived at the fourth visit.  No pain, full motion, strong, highly functional at home and with hobbies.

Most of you reading this have been there.  We pray this patient maintains this status and we don’t want to be the bad-news “physical torturist” because sometimes they are functional for a long time this way.  Knowing his reluctance to work outside the realm of he and his surgeon’s normal, I stood down.  He had met all of his goals, he did have functional strength, motion and his goals were met.  I simply reminded him that I had done very little, that there was likely still a root cause of this now-recurring left shoulder dysfunction, not to feel hopeless if it did ever recur, wished him my best and discharged him—physician and patient goals met.  

For now.

I’m interested in your feedback, stories, predictions for part III, anything you'd like to add to this little story so far.  Again, this is outlining a classic case where the road less traveled is a bit risky, and in this case I took the easy way out with some objective data to support my decision. 

Part III coming soon…

Myokinematic Restoration originally scheduled in Spokane, WA, has been moved to Seattle, WA on May 31-June 1st! There are still a handful of seats available, so if you are in the Northwest, be sure to register soon. The early registration rate of $445 has been extended until next Wednesday, May 21st!

 

It looks like we are going to have beautiful weather for our 6th Annual Interdisciplinary Integration Symposium this week. Safe travels to Lincoln!

This was the second time that I had the pleasure of teaching at Finish Line Physical Therapy in New York City, and I am always grateful for their genuine appreciation and interest in PRI. After a weekend of Postural Respiration, I know most of them will not forget how to integrate left abdominals with left posterior mediastinum and right lateral thoracic expansion. I hope they became "lifted" as much as they "lifted" me on a wonderful rainy weekend in New York!

Impingement & Instability (Woodbury, MN) – “Karen and Carrie and the staff at Kinetic Physical Therapy Institute were fantastic hosts for a wonderful weekend of Impingement and Instability. It was great to spend the weekend with 2 clinicians I have always respected and appreciated dating back to before we went through the PRC process together back in 2004. It was great to reflect back on the development of PRI’s courses, including the new updates and developments to this Impingement and Instability course. We had a dynamic group of PTs, PTAs, Fitness and Strength professionals, 5 PRI Credentialed Professionals, a dynamic Sports Medicine minded Family Practice Physician and my favorite, an Engineer who is pursuing fitness and performance as a second career. It was clear that being an Engineer was a definite asset that helped Jacob understand the three dimensional integration of movement that is such an important part of understanding PRI. And Dr. Dave, you are easily one of the most open-minded and interested physicians that I have ever met out on the PRI circuit. A physician that regularly assesses his patients for body asymmetry and an imbalance of movement in spite of their symptoms is very uncommon. Your insights as a physician with experience training the US Ski Team was really an asset to our discussion on ischial tendonitis. A couple other take home messages from this weekend were to always ask if your patient’s ribs move the way they should to allow for tri-planar body performance and to remember the value of training right trunk rotation when you are standing on your right leg. The group did a fantastic job incorporating advanced concepts in a way that will allow them to balance neurology and performance on a wide variety of patients and athletes.”

Some of you might have recently seen this video trending on Facebook and Twitter, and I am thrilled to see that it is available to view on the NSCA website! Last January, Ron Hruska and Mike Arthur presented at the 2013 NSCA Coaches Conference in Nashville, Tenessee. Their presentation was titled Postural Restoration: A New Tool for the Coaching Tool Box. To watch this presentation, CLICK HERE!

There are a few seats available for the rescheduled Postural Respiration course in Portland, OR on February 22-23, 2014! Click HERE to get signed up today!

“What Introductory PRI Course Should I Take First?”

Hello PRI world of thinkers and learners!  Jesse Ham here, chiming in on a topic that has been and will continue to be a worth-while discussion:  What is the best way to get clinicians engaged into looking at movement through a PRI lens?  Or, put another way, what PRI introductory course will be the best to take first?  There really isn’t a right or wrong answer.  This is my impression from my experience personally as a clinician and from listenting to others' responses after they have taken various courses.

If we were all blessed with Ron Hruska’s ability to shift paradigms, take in seemingly limitless amounts of information, integrate it together and apply what we learned, then there would be a simple solution.   We would all take a week-long PRI Introductory course called Postural Myokinematic-Pelvis-Respiration Restoration.   Not only does this title not fit on the front of a manual, it’s a mouthful to pronounce, much less digest and apply all at once.

Even if we could get a week off consecutively to attend such a course, most of us will be on “new information maximum” somewhere between the afternoon of the first day and mid-morning of the second day.   After taking my first Myokinematic Restoration Course “four score and seven-plus years ago,” I recall the need to work with it on many patients, review the manual, PRI blogs and emails, and just process the base concepts for quite some time.  So, since the best introductory course is a bit bulky, I pose a feasible strategy for where to begin taking the three introductory courses, Postural Respiration, Pelvis Restoration and Myokinematic Restoration.

To do so, I will take a small tangent here:  Before I was aware of this Institute, in fact before I went to PT school,  I was aware that clinicians struggled mightily treating IS (Ilio-Sacral) joint dysfunction.  There were seemingly as many special tests and strategies for treating this joint as there were clinicians and instructors.  Some said the IS joint didn’t move at all, others said it needed to be manually mobilized if it wasn't functioning properly.  Every static and dynamic imaging study had been done, with conclusions that gave very little insight from a clinician’s standpoint.  I studied Cyriax and all the derivatives up to Mulligan's work presently, I studied Gary Gray’s viewpoint.  I reviewed the various clinicians’ work who were, in part, responsible for muscle energy techniques to continually self-mobilize the ilium on the sacrum.  There are many more who contributed to this IS joint's body of research and treatment techniques, I have merely brushed over a few.  The take home here is that after PT school and several years of practice, I had no definitive answers as to how to affect the position of this joint and maintain that effect for my patients as they moved in a triplanar world of forces.

Then I started to take on the world of PRI and its viewpoint as to how to effect this IS joint's position.  As I became more adept at utilizing PRI concepts, I was far more successful at treating maladies related to IS dysfunction.  But there were still some patients that I had to constantly reposition, those who were never free of a relatively constant “HEP.”  Far too many (~20-25%) of these patterned IS dysfunction patients were “better” but not well.  They still needed consistent intervention, were not integrated and therefore I was not happy.  Loose ends and unanswered questions still bothered me for some of my IS patients.

Along came Lori Thomsen and later Jen Poulin teaching Pelvis Restoration.  Mind you, the concepts of pelvis position are woven into Postural Respiration and Myokinematic Restoration, and this discussion does not apply strictly to IS dysfunction–that was just one of my conundrum diagnoses that I use as an example here.  But from my experience I was not as effective at those “tough ones” that we all have until I began to appreciate the position of an inlet and an outlet of a pelvis.  Specifically, how that inlet and outlet position enables me to integrate a thorax with lower extremities optimally to allow a patient to attain reciprocal, alternating function and live their lives free from the bondage of perpetual, unsustainable diagnosis-specific exercises to maintain their function.

The above is my abbreviated rationale to the question I posed for the title of this piece.  For those of you who skipped to the end of the book and like short answers, mine is this:

If I had it to do again, I’d take Pelvis Restoration first, followed relatively closely by Myokinematic Restoration and Postural Respiration.

Thanks for taking the time to review this blog.  I will enjoy reading your experiences and story about what introductory worked well for each of you!