Orthopedic Physical Therapy

Onward and Upward!

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Wed, 1 Apr 2009 20:26:00 -0500

Well folks. I really have enjoyed the Blogger format to this point and it has served me very well over the past year. In fact, I'm enjoying the process so much I started the Movement Science Podcast hosted by Podbean, and have even joined forces with Eric Robertson at the PT Think Tank.

With this said, I have found a new home for the blog on WordPress. The next evolution of "Orthopedic Physical Therapy" will be the Movement Science Blog and Podcast. At this time WordPress seems to have a really nice format that offers me some additional flexibility for integrating both the blog and podcast together in one website. It also has a very user friendly interface I believe you will enjoy once it is fully up and running.

The format will be essentially the same as it has been for the past year on this website. I will be discussing issues such as:

Rehabilitation Science
Exercise Science
Orthopedic Medicine
Neuroscience and Motor Control
Current events relevant to the fields of movement science

I am officially knee-deep in my doctoral studies at Texas Tech and with the IAOM, so I hope you will continue to join me on my journey to better understand the amazing processes that govern human movement. As time goes on, I hope to integrate more research, more interviews, and hopefully challenge you to never stop learning.

I am still getting acquainted with the format over at WordPress, but I hope you will visit me there and continue to follow this blog in its new format. I will continue to put my posts here on Blogger until the official turnaround at the end of April. In the meantime, I will have all my new and old posts and podcasts on both sites.

So to wrap this up: I'm moving but will take it slow and post regular updates until the final transition to Movement Science at the end of April 2009. Also don't forget to visit the PT Think Tank and interact with me there as well. In the meantime, take care and I hope to talk with you soon!

Good stuff from the APTA on manipulation

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Fri, 20 Mar 2009 17:27:00 -0500

This is a quick-hitter post I thought some of you out there might find interesting. I recently had a pleasant but slightly contentious discussion with a local chiropractor that wandered off into the topic of manipulation and scope of practice.

"I find it curious that PTs are so eager to criticize chiropractic, yet are equally eager to manipulate."

- Dr. Unnamed Chiropractor, DC

First of all, let me please go ahead and thank God for the ability to guide my emotional and physical restraint. Were I a younger man this is something that would have put me over the edge. Fortunately I was able to sit on my hands and restrain my tongue long enough to calmly discuss the issue with him. My talking points included:

The physiology of manipulation (i.e. its role as a self-perpetuating "adjustment"versus a means to normalize function).
The messages of self-restoration in physical therapy compared to chiropractic (I know - this is the supposed mantra of the chiropractic profession. I guess you only need a lifetime of adjustment before realizing this self-correction...)
Unsubstantiated claims regarding risk of a manipulation performed by a physical therapist

The conversation was brief, but I felt amazingly well prepared. Best of all...I carried it off with a sense of satisfaction that I did the right thing for our profession in sending a message to the chiro that we are well trained to perform thrust-mobilization (manipulation) and have a better model of care to support its use.

Right on the heels of this conversation, I received an email from the APTA which I strongly suggest you review if you are close to this situation. The email was from our Advocacy section and outlines some great presentations and handouts regarding PTs and manipulation. I'm a vocal critic of my organization on some issues, but man they do some great things with our dues. It is a tough check to write each year, but I feel more strongly it is the right thing to do everytime I get one of these emails. This will be a great resource for us for some time to come.

P.S.

Thank you all for the great responses to my first podcast! They were greatly appreciated. Stay tuned and I've got some really good topics on the way. Also, I may be updating the format of my blog to be more user friendly and offer easier access to archived posts and my podcasts. Hang in there and we'll continue to grow!

Movement Science Podcast: On the Air!

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 15 Mar 2009 11:29:00 -0500

Ok folks here we are - my first podcast. This episode explores the relationship between motor learning, motor control deficits, and low back pain. I hope you enjoy my rookie effort and will hang in there as I continue to improve this new feature of my blog. Please let me know if you are having difficulty dowloading the podcast and I will get the bugs worked out asap! I hope to be up on iTunes soon so this should add an additional level of functionality to the show.

Topics include:

Recent editorials in the BJSM on the role of lumbar stabilization in low back pain
Basic motor control theory and the process of motor recovery following an injury including a reduction in cognitive regulation, decrease in visual dependency, and improvements in sensorimotor adaptability
How pain influences motor behavior including local and affective influences on muscle activity
An overview of what we know and don't know regarding motor control interventions
How this information has influenced my approach in the management of low back pain

Articles cited:

Allison, G., & Morris, S. (2008). Transversus abdominis and core stability: has the pendulum swung? British Journal of Sports Medicine, 42 (11), 630-631 DOI: 10.1136/bjsm.2008.048637

Hodges, P. (2007). Transversus abdominis: a different view of the elephant British Journal of Sports Medicine, 42 (12), 941-944 DOI: 10.1136/bjsm.2008.051037

Cook, J. (2008). Jumping on bandwagons: taking the right clinical message from research British Journal of Sports Medicine, 42 (11), 563-563 DOI: 10.1136/bjsm.2008.048629

Mulder T, Neinhuis B, & Pauwels J (1996). The Assessment of Motor Recovery: A New Look at an Old Problem J Electromyogr Kinisiol, 6 (2), 137-145

Hodges, P. (2003). Pain and motor control of the lumbopelvic region: effect and possible mechanisms Journal of Electromyography and Kinesiology, 13 (4), 361-370 DOI: 10.1016/S1050-6411(03)00042-7

Young Guns

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sat, 14 Mar 2009 17:29:00 -0500

I just wanted to say congratulations to a few former students of mine who recently earned their licenses. They graduated from UTMB back in December and are all gainfully employed! I was very fortunate to have them as students and am now privileged to call them colleagues. Congratulations and best of luck to Anne, Andrew, and Ryan. I'm very proud of you all and wish you all the best.

Rod

Put down the barbell and slowly back away...

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sat, 14 Mar 2009 17:03:00 -0500

This may get me in a bit of trouble but here I go. Many colleagues have taken issue with my stance on the role of physical therapists in the realm of exercise as well as strength and conditioning.

My stance is simple and begins with a simple observation: Physical therapists are the undisputed experts of rehabilitation science. Rehabilitation is a sub field within the broader category of movement science and is accompanied by other sub fields such as biomechanics, exercise physiology, neuroscience, motor control, and the like…

As sole title holders of "World Champions" of rehabilitation, exercise physiologists and biomechanists cannot and should not declare themselves rehabilitation experts. This observation is plainly obvious to most physical therapists (just ask one). We are happy to share this with anyone who is willing to listen as well as some who aren't.

So why then do we in physical therapy get so befuddled when those specializing in exercise science question our role in prescribing exercise programs for athletes and otherwise healthy individuals?

A recent discussion on the RehabEdge forum took place in which we debated the merits of athletic trainers in treating a nonathletic population. Without getting into the specifics of the debate, it was generally agreed that physical therapists can’t hold a trainer’s jock (so to speak) in the assessment and management of an acute athletic injury. At the same time we argued that trainers can’t hang with a PT in the majority of rehabilitation settings. To put it succinctly, while there is some overlap in skill set, there is clearly only one professional best suited for the job. Of course, many therapists and trainers are duly credentialed in both fields….all bets are off for you!

We aren't bad...but there is better.

Physical therapists, like doctors and other health care professions, should feel a natural pull toward providing general activity guidelines for patients. In this regard our role in healthy movement should not be underestimated. However it will be difficult to press on and be great in rehabilitation if we are trying to be all things to all people. There is a professional best suited to provide exercise advice and leadership, and it is not us.

Now would be a good time for a wary reader to point out my arrogance in claiming to be both. This would be a fair criticism, but for better or worse, I have graduate degrees and extensive training in human performance and physical therapy. Like those credentialed in both athletic training and physical therapy, I hold titles in both sub fields. With that said, it is tough for me to be good at both. I’m probably a much better physical therapist right now than I am strength and conditioning specialist. That’s OK though…my patients probably would want it that way!

Want to be an expert? Here's how to earn it...

So here’s my official position and recommendations for physical therapists wanting to become exercise professionals:

· Physical therapists are not exercise specialists and should lay limited claim to human performance training unless specific criteria are met.

· The first criterion is achievement of an advanced certification from either the American College of Sports Medicine or the National Strength and Conditioning Association. Sorry to the pretendors that I carefully excluded from this list. These two organizations represent the highest standards of the profession and offer numerous opportunities for increasing knowledge of exercise science.

· The second criterion is a graduate (preferred) or undergraduate degree in exercise physiology or related curriculum. This will provide a solid and specific academic background in exercise science. You can attempt to tell me a physical therapy curriculum is sufficient to achieve this knowledge, but you would also be wrong.

· In the absence of meeting either of the above criteria, the physical therapist should spend at least 2-3 years working in a fitness and human performance setting with a seasoned conditioning specialist. I have a tough time with this one, but realize that it isn’t easy to achieve both of the above criteria. Trying to give a little here…

Bottom Line

If you believe my recommendations to be unreasonable I would challenge you to have a discussion on a specific issue pertaining to exercise science with someone who has met the above criteria. You may think you have sufficient knowledge and understanding of exercise physiology and human performance, but the conversation may cause you to think twice. I strongly encourage those in the rehabilitation profession to do what you do best. If you want to be considered an expert in physical therapy, you know where to go. If you goal is to hold expertise in exercise as well, please apply the same rigor to your standards as we expect from other professions.

P.S.

The first podcast is currently “in production” and I hope to have it up and running soon faster than I expected. Thanks for visiting and I’m looking forward to talking to you soon. If you have a question or comment, please don’t hesitate to contact me and I’ll try to address it on the podcast. Take care.

Class Dismissed...

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Tue, 10 Mar 2009 04:55:00 -0500

Just got back from Lubbock and feel like a charged capacitor...

There are so many thoughts and ideas running through my brain that it will be a true test for me to sit still long enough to articulate them. Fortunately my wife, blog, colleagues, and my upcoming podcasts will give me a nice steady discharge of this energy as opposed to blowing all at once!

The origin of my excitement is my experience at a recent contact session for my Sc.D. program at Texas Tech. The title of the course is "Motor Control in Orthopedics" and is basically part two of last semester's "Neuroscience in Orthopedics" course. The weekend began with a review of the motor control principles we independently studied over the last eight weeks. Information processing, attention and memory, peripheral and central contributions to movement, motor learning and practice...these were all reviewed and discussed with our course (and program) director Phil Sizer.

The second component of the course jumped over into practical application where we discussed issues pertaining to motor control and syndromes of the cervical and lumbar spines, shoulder, knee, and ankle. The vast majority of slides and resultant discussion stemmed from the peer-reviewed works of people like Hodges, O'Sullivan, Powers, Hewett, Falla, Jull, Flynn, Childs, and many MANY others. From this standpoint, the information presented was a good representation of the state of motor control as it pertains to our profession.

This information was juxtaposed with Phil's infectious passion for the material and synthesis. The result was the generation of great (raw...but great) ideas regarding management from my fellow classmates. I have to say from this perspective it was very inspirational. I will admit my threshold to excitation is a bit on the low end at times, so take that for what it's worth...

NOW. There were a few occasions on day two where I seemed to scratch my head. As positive as I am about the course, I have some questions/concerns about our integration of these topics. Predictably my concerns pertain to things like the relevance of feedforward TrA activation, hip weakness in anterior knee pain, etc...

What is the relationship between lumbar muscle dysfunction and LBP? We know the relationships are there, but identification is not sufficient to place them in proper perspective. Despite our eagerness to dive into and "treat" these areas with various activity programs such as "core training", a stricter adherence to principles of motor control may cause us to rethink our current approaches. (more on this soon!)

What are the relationships between hip muscle strength and anterior knee pain? We often see measurable decreases in hip capability in the presence of knee dysfunction. However this observational statement is only the beginning. Is this relationship causal or simply correlative? If it is causal, are we confident which came first? The answers have not been clearly defined and have profound implications for evaluation and management.

I believe the answers will become clearer as we begin to integrate clinical observations (weak hip abductors, functional instability, etc...) with our emerging understanding of neuroscience and motor control. Over the next several weeks, I hope to present examples and arguments in favor of integrating these fields of movement science and the evolution of understanding that they can bring. I am excited to share this with you and look forward to your questions and comments!

Can you hear me now?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Tue, 24 Feb 2009 23:17:00 -0600

Ok folks...I'm not fully satisfied with my current status as PT-nerd extraordinaire, so I am taking this to the next level. You guessed it: podcasting has made its way to my blog. The blog's title is a work in progress but is tentatively known as the Movement Science Podcast.

During my recent post on Ginger Campbell's blog, I was struck with this idea to create a podcast that deals with issues pertaining to movement science. Physical therapists, exercise physiologists, biomechanists, physiatrists, orthopedists...we all deal with human movement at varying levels of function or dysfunction. My hope this podcast will be able to reveal and discuss some of the incredible work that is being done in the name of helping us move around on this earth a little better. Our topics will include (among others)

The role of rehabilitation science in reversing orthopedic and neurological movement dysfunction
The role of physical activity in improving both physical and cognitive health
Training concepts for strength and conditioning professionals and rehab professionals who want to become better strength and conditioning professionals!

The format will range from interviews, discussion of relevant literature, and of course some home spun editorial from the author! Please excuse the amateur effort as I troubleshoot getting the podcasts onto my blog and eventually into easily accessible formats such as iTunes and the rest. It is my sincerest hope that this can develop into something great. If you work in movement science and have an idea for a podcast you'd like to hear, feel free to drop me a line and become a part of the process.

Exercise and the Brain

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 22 Feb 2009 19:08:00 -0600

During a recent Skype phone call with fellow blogger Diane Jacobs, the discussion of physical activity and motor control came up. Diane is noteworthy for having an opinion or two on the role of neuroscience in the world of physical therapy, but what I've come to realize is she's equally eager to help colleagues learn and will go out of her way to do so. Thanks again Diane.

After the phone call, Diane sent me a link to one of Ginger Campbell's Brain Science Podcasts. The podcast is an interview with Harvard physician John Ratey and his new book Spark: The Revolutionary New Science of Exercise and the Brain. It is a fascinating interview and it sounds as if the book could be an equally fascinating read. I was particularly fired up to hear Dr. Ratey's take on exercise and neuroplasticity. He actually refers to exercise as "the undisputed champ of neuroplasticity for the brain". What a powerful statement that could have incredible and far-reaching implications for the role of therapeutic exercise in our clinical outcomes.

Please feel free to check this podcast out and let me know what you think.

If you are interested in learning more about Ginger Campbell or listening to more of her podcasts (she's got a great southern accent by the way) feel free to check out her website. I will also add it to the list of "Great Medical Blogs" on my site.

The elbow's connected to the...Brain?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Mon, 16 Feb 2009 06:19:00 -0600

If you've been reading my blog for a while, you've probably picked up on my fascination with neuroscience as it pertains to orthopedic dysfunction. For better or worse, the neuro-theme continues as I am now immersed in topics pertaining to human motor control. As usual, I am having more fun than I should be allowed to have...

Today's journal article comes to us from the Archives of Physical Medicine and Rehabilitation on the topic of lateral elbow pain. Lateral elbow pain continues to baffel the medical community. This should come as little surprise when you examine the relative paucity of quality research devoted to this troublesome condition.

Sensorimotor deficits have previously been documented in patients with lateral elbow pain. Despite treatment measures aimed at addressing pain and function, no studies have examined whether conservative measures address sensorimotor deficits in the short or long-term. The primary objective of the present study is to examine the effect of physical therapy and corticosteroid injections compared with a wait and-see (natural history) approach on sensorimotor function.

Design

The study design was a single-blind randomised clinical trial. Outcome measurements were taken at baseline, six-weeks, and finally at a 52-week follow up. An initial population of 497 individuals were considered for the study. Exclusion criteria were bilateral lateral LE, concomitant shoulder or neck complaints, treatment within the last ten months, or other elbow problems. This left 198 subjects available for randomisation. Sixty-seven were randomised into a wait and see group. Sixty-five were randomly assigned into a corticosteroid injection group. Sixty-six subjects were placed in the physical therapy intervention group.

Methods and Intervention

Subjects in the wait-and-see group were given ergonomic advice on how to modify activity and avoid aggravation of their symptoms. Subjects receiving the corticosteroid injection were administered a local injection of 1mL lidocaine with 10mg of triamcinolone at baseline with advice to gradually return to normal activity. The physical therapy group consisted Mulligan’s Mobilization with Movement technique along with a graded exercise program over an eight week period.

A series of reaction time tasks were performed using a standardized instrument called the Sensorimotor Interface Hand Module. The tasks consisted of an standard reaction time for one choice (SRT-1) and two choices (SRT-2). Reaction times and speed were measured for both upper extremities. These outcome measures were taken at baseline and at 3, 6, 12, 26, 52 weeks. Short-term outcomes were defined at 6 weeks with long-term results at 52 weeks. Estimates of effect were measured using a three-way analysis of variance with time, treatment group, and side (affected vs nonaffected). In addition, the LE group was compared to a healthy control group (n=40) at all time points.

Results and Conclusion

All measures of reaction time in the LE group were significantly impaired in both UE compared to normative values at baseline (P>.001). These impairments persisted at all time frames including both short and long-term follow ups. The sensorimotor deficits between all treatment groups were similar at baseline, short and long-term follow ups.

Sensorimotor deficits are evident in patients presenting with LE compared to healthy controls. These deficits persist over a 12 month course of treatment regardless of the intervention. There was a tendency for reaction time to normalize within the initial six-weeks in the treatment cohort, but this effect was not significance and reached a plateau beyond this point. The authors speculate that changes in central sensorimotor processing explain the persistent impairments in reaction time. Central changes may also explain the bilateral deficits in patients with LE.

My Take Home...

The present investigation represents a powerful example of the nervous system’s role in musculoskeletal dysfunction. Sensorimotor function is significantly impaired in patients with elbow pain, and this deficit persists over a long period of time regardless of the treatment. Moreover, these deficits were reported to persist regardless of fluctuations in the patients pain or reported levels of disability. Interestingly, the authors did not utilize pain or disability measures as an outcome measure. This was a significant limitation of the study in my mind.

Despite the limitations, the findings may partially explain the high recurrence of conditions such as lateral elbow pain, and may be useful when considering any patient who has had chronic or persistent joint pain. Therapists may want to include measures of sensorimotor function when evaluating patients with painful conditions.

The implications of this investigation are pretty significant in terms of our assessment and management of not only lateral elbow pain, but other chronic conditions as well. As usual, research like this leaves me with more questions than answers. For example:

Just how prevalent might sensorimotor deficits be in other chronic conditions commonly seen in our clinics?

When throughout the course of the disease do these sensorimotor deficits begin to emerge?

Do the deficits occur secondary to chronic pain or are they the primary deficit that predisposes individuals to particular conditions?

Are specific interventions capable of addressing these primary or secondary sensorimotor deficits?

As always, I welcome your thoughts, questions, or contributions on this or any of my other blog posts. Stay tuned as we continue to delve into topics pertaining to practice patterns, low back pain and imaging studies, clinical neurodynamics, and a host of other topical issues pertaining to orthopedic physical therapy!

L BISSET, M COPPIETERS, B VICENZINO (2009). Sensorimotor Deficits Remain Despite Resolution of Symptoms Using Conservative Treatment in Patients With Tennis Elbow: A Randomized Controlled Trial Archives of Physical Medicine and Rehabilitation, 90 (1), 1-8 DOI: 10.1016/j.apmr.2008.06.031

Great Webinar from the NSCA

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Wed, 28 Jan 2009 19:57:00 -0600

I've never taken the opportunity to attend a webinar, but I thought I would share the experience of a recent online lecture hosted by the NSCA. The webinar titled "Strength and Conditioning for the Endurance Athlete/Sport" was conducted by Greg Haff, PhD, CSCS from the University of West Virginia.

As a pretty finicky consumer of continuing education, I have to say this was a well organized and evidence-based discussion regarding the benefits and limitations of various strength training methodologies for the endurance athlete. Dr. Haff even addressed popular "core training" regimens and their dubious effectiveness in improving performance. Without ripping off his lecture completely, here are a few gems I picked up from the webinar:

A well-planned resistance training program is capable of improving endurance performance. This has been consistently demonstrated in activities ranging from running to cycling and swimming.

An important corollary is that endurance training does NOT benefit the strength athlete!

Resistance training should not simply be added to the total training time. Otherwise, cumulative fatigue may likely negate potential training benefits or expose the athlete to injury. Consider replacing some of the endurance training load with resistance training. Of course, seasonal variations should be considered here.

Focus on compound movement patterns that appear to have maximum specificity to the activity.

Core training appears to have little to no benefit for endurance training.

In one of my earliest blog posts, I resolved to return my efforts to my roots in exercise science. This webinar certainly helped stoke these fires. This year I will be blogging on issues pertaining to exercise science. In particular I will focus on the sometimes controversial role physical therapists have in this highly specialized field. I have strong opinions about the role of PT's in strength and conditioning and hope the posts will inspire those in our profession to seek a greater understanding of exercise science. Until that time, take care and talk to you soon!

Thanks Chad...

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Wed, 21 Jan 2009 21:20:00 -0600

I need to give some much-deserved props to Chad Brinkmann, a physical therapist whose recent letter to the editor in the January 2009 edition of Advance reaffirmed my attitude about the DPT and Vision 2020. While I encourage you to read the full letter for yourself in the magazine, I have to echo some of Brinkman's points and offer them up for discussion or opinion.

The APTA has added to the debt load of physical therapy students by pushing the DPT in the absence of any significant difference in pay. After doing some very simple math, students are fleeing to other professions.

This potential reduction of qualified individuals in the workforce will inevitably lead to an imbalance between the supply and demand of our services. Fewer therapist treating more patients is not the recipe for quality treatment.

The DPT could completely devalue the need for the PTA. Third party payers play "follow-the leader" all too well and will inevitably cease reimbursement for PTA services. Don't think it could happen? Feel free to give me good reasons why they wouldn't. Reductions in the numbers of working PTA's spreads the caseload even further!

I don't believe the DPT is an awful way to go, and sincerely respect my colleagues who have earned the credential. I have more than a few DPT friends who will likely rip me pretty hard for this post. However, it is appearing more and more that the APTA tested the water by jumping in with both feet on Vision 2020. In our obsession with becoming a "doctoring profession" we have lost site of the realities our our practice today.

I rejoined the APTA last year and plan on renewing my membership again and again, but I think it is important for us to join Chad in voicing our opinions about the direction we should be heading. Having a vision is one thing, but I think we developed a case of hyperopia in the process. I join Chad in encouraging the APTA to make Vision 2020 a fluid one in which the goals of our profession in eleven years reflect the realities of today.

Good on'ya Chad...

Overuse Injuries: Time for a top-down approach?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 4 Jan 2009 08:52:00 -0600

I've been running (well jogging) for five years now. During my first job as an administrator in 2004, I had developed a nice little case of hypertension, gained 10-15 pounds, and was generally unhappy and most likely unpleasant to be around. After what many from the southern states refer to as a Come-to-Jesus meeting with myself, I decided something had to right the ship lest it strike an early infarction-berg in a sea of weak metaphors.

I get many of my blog ideas while running. You may be surprised to know how much random thought a cortex can generate with blood pumping through it at 150 beats per minute. I began thinking about how lucky I am to be training as much as I do, but have yet to encounter an overuse injury. Overuse injuries sidelined my first attempt at training for a marathon back in 2000 in the form of heel and medial knee pain. I have been eager not to repeat my mistakes of the early millennium, and fortunately (currently knocking on wood) have avoided any roadblocks.

Many of our patients in an outpatient orthopedic setting haven't been so fortunate. Activities such as running, bicycling, and swimming can be physically demanding enough to overwhelm a vulnerable weak link within the patient. It is very likely that the body does its best to compensate for this vulnerability. However, just as in life, in the absence of a fundamental change in training load, a weak link is nearly always exposed. In the case of physical activity, the stereotypical "overuse" injury results.

Mechanisms of Overuse

Overuse injuries can occur for a variety of reasons including a premature increase in training load (distance, speed, intensity) or inadequate recovery between bouts of activity. Most injuries are capable of healing in the standard inflammatory-nociceptive pattern if afforded the right environment.

However if you've treated what some refer to as obligatory exercisers, you'll realize that some folks have a tough time giving themselves the best opportunity to heal. The condition transitions from medial knee pain to chronic medial knee pain. Even more frustrating for the patient is that the medial knee pain will persist despite reductions in training load and attempts at standard and even non-standard rehabilitative care. Pain may begin occurring at lower training thresholds or even at rest, leaving the patient feeling painted into a corner of inactivity. It doesn't take long for frustration to deteriorate into depression and eventually dropout.

It's important to note that even the best training programs and access to care will not prevent some injuries. If that were the case, professional athletes would never develop an overuse injury. The ones that do would be rapidly rehabilitated and miss very little playing time. Obviously even professional athletes encounter these kinds of issues, and suffer greatly for them. This despite well planned primary preventive and treatment programs.

Current Models

Let's face it, we all understand the inflammatory process and concepts related to overuse. We are capable of explaining these concepts to our patients and assuring that they understand the means to avoid overuse injuries. Yet these problems continue and occasionally flourish! I propose taking a hard look at how we manage these injuries with the following observations in mind:

Chronic overuse injuries often persist well beyond cessation of the precipitating activity such as running or throwing.

Overuse injuries often persist in the presence of normal strength, flexibility, and normal variations of posture and biomechanics.

Overuse injuries such as lateral epicondylalgia and anterior knee pain often show no clinical or histological signs of a local inflammatory process.

The pain associated with overuse may persist following a well-planned rehabilitation program consistent with our current standards of care.

Top-Down

Recent evidence suggests that the longer a painful condition exists, the less likely it will behave as a traditional inflammatory/nociceptive condition. It has been fairly well-established that peripheral and central neurophysiologic mechanisms can maintain a condition long after the tissue has healed. Factors such as up regulation of receptor volume at the site of injury, dorsal column, and even supraspinal regions make central sensitization a likelihood for chronic overuse injuries. The trouble is how to incorporate an understanding of these events into our treatment plans?

Unfortunately, this isn't a simple matter. We are just now (over the last 10-15 years) years) becoming aware that central mechanisms play a role in the maintenance of these conditions. As a result there are scant outcome studies and no CPRs. All we can rely upon right now is the best available evidence, our clinical judgement, and the interests of the patient to guide our interventions. My own approach is to educate the patient about the local and central physiology of their chronic condition. Education has been a fairly well established way to manage disability in patients with persistent low back pain, and I believe their is some carryover in the "overuse" population.

The focus of my education is along the same line as David Butler's user-friendly educational book Explain Pain. It starts with a very simple explanation of what causes the initial onset of pain and the mechanisms of how it can become chronic. Having a clear understanding of the physiology of pain is helpful here because the patient will often ask many very good questions.

There are two very powerful benefits to this approach. Firstly, the patient loses the notion that "something MUST be wrong". Often these folks have been told that there are minimal radiographic or clinical findings to correlate with their symptoms. This often leaves the patient with a sense of dread regarding their condition's prognosis. You can relieve this stress through a fairly straightforward educational session about the mechanisms of their pain. The patient leaves the session with a sense of understanding and confidence about their potential to recover from their condition. The physiologic mechanism behind this process includes supraspinal descending inhibition through structures such as the periaquiductal grey, anterior cingular cortex, and amygdala of the brain. These structures are felt to be responsible for the analgesia produces by events such as positive expectation, placebo, and other psychosocial factors.

Secondly, the patient now has a well-informed basis for action. This has tremendous advantages in that the patient will be less likely to undermine your care plan when they aren't in the clinic. There is strong evidence to suggest an informed individual will engage in conscious and subconscious movement patterns that foster a good healing environment. This will allow for a more complete resolution of damaged tissue and reduce the likelihood that pain will persist. The patient will eventually take a more logical approach to their activity progression and maintenance. The end-result is an informed patient who has all the skills they need to get out of their current condition and reduce the likelihood for a relapse.

Effective Education

This educational probably isn't entirely different from what many other therapists are doing in their clinics, but I believe it does require some effort. Not every patient has the same educational background and learning style. As a result, your teaching methods will need to vary considerably between patients. Secondly, it requires the therapist to have a well-developed understanding and integration of the inflammatory process, pain science, and principles of training and conditioning. A more complete understanding of these fields can be very beneficial for patients suffering from chronic overuse injuries.

I hope this glimpse into my approach to this troublesome condition is useful for you mainly as a primer for further study into these disciplines. It has definitely helped my practice over the last year. After submitting this entry, I'm going to walk outside and try to set a personal record in my 10K. Wish me luck and an injury-free morning!

Take care and feel free to comment on this or any other blog. I always welcome the discussions.

Are you an expert clinician?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 28 Dec 2008 08:22:00 -0600

If you've been reading my posts for a little while now, you might have noticed I place a high value on education. I've been teaching as an adjunct instructor for over eleven years at a local university and regularly take students on clinical rotation. After a recent four-week (entirely too short) rotation with two year-one PT students, I found myself looking back on to their experiences at the clinic and wondering what I could have done better. They both had a great experience, but I couldn't help but wonder why I wasn't quite settled with the approach I took with them.

I began looking into clinical education models across several disciplines and found there is actually quite a bit of literature out there on the subject. One article in particular caught my mind regarding the differences between what's considered to be "novice" and "expert" clinicians. I was curious for a couple of reasons. Firstly, I wanted to know if my expectations of the students were matched appropriately to their skill level. For example, how can I bring a year-one along compared to the more advanced students without either frustrating or overwhelming them? Secondly, I was pretty curious to see if, despite my experience and board-certification, I could consider myself as an expert!

Today's article comes from the PT Journal back in 1992. The articles author, Mark Jones, provides a very straightforward discussion of clinical reasoning and the nature of expertise. Since the authors/editors of these articles do a much better job of outlining their ideas than I do of encapsulating them into my blog, I have provided a link to the full text article here.

Defining Expertise

Traditional notions of expertise have related to experience. Students were often considered novices while advanced practitioners were considered experts. While this may often be the case, a more precise delineation of what constitutes expertise may be useful. The author contends that expertise be considered along duel continuum of both generic and specialized knowledge. A sub expert is someone who possesses adequate generic knowledge, but insufficient specialized knowledge of a given domain. Predictably an expert possesses both generic and specialized knowledge of the domain.
An expert is distinguished through utilization of superior organization of generic and specific knowledge, hypothetico-deductive reasoning, and pattern recognition.

Expert Practice

Clinical reasoning will be influenced by a combination of the therapist's knowledge base along with their cognitive and meta cognitive skill set. Cognitive literature suggests that these components can be improved with effort, but can suffer through neglect. This indicates that the most expert clinical reasoning comes from not only knowledge, but the ability to step back and examine our cognitive biases when dealing with a case. Additionally, the reasoning process can only be as good as the collected information. It is critical that the clinical environment be designed in such a way to optimize the collection of accurate and reliable information from the patient. Our busy clinics can impose obvious limitations on the information gathering process such as group norms, time limitations, unrealistic productivity standards, and overextended case loads.

Teaching Students to Become Experts

Obviously, getting a student to become an expert is a tall order and not entirely realistic. However, we can teach the students to exercise their clinical reasoning muscles (i.e. the brain) by challenging them to go beyond the books in determining the best course of action. As Jones puts it:

Facilitating students' clinical reasoning requires making them aware of their own reasoning process and designing learning experiences that promote all aspects of the clinical reasoning process while exposing the errors in reasoning that occur. This requires access to students' thoughts and feedback on thinking processes. That is, students should be taught to think and to think about their thinking. This can be achieved by promoting students' use of reflection to encourage awareness and promote integration of existing versus new knowledge. When combined with a better awareness of one's own cognitive processes (ie, metacognition Metacognition refers to thinking about cognition (memory, perception, calculation, association, etc.) itself or to think/reason about one's own thinking. Types of knowledge ), the students' processing of information is enhanced and clinical reasoning is facilitated. Learning experiences to facilitate clinical reasoning using both reflection and metacognition are described elsewhere.

The process of reasoning should not, in my view, be addressed to the neglect of knowledge. Rather, facilitating the clinical reasoning process will assist the students' acquisition of knowledge. In turn, good organization of knowledge leads to better clinical reasoning. The importance of one's organization of knowledge is closely linked to the accessibility of one's knowledge. Knowledge that is acquired in the context for which it will be used becomes more accessible. Although clinical knowledge is typically presented in the context of patient problems, this is less commonly the case with the basic sciences (eg, pathophysiology). Approaches to physical therapy education in which the acquisition of knowledge is facilitated by teaching centered on patient problems provide, in my opinion, the ideal environment for building an accessible organization of knowledge and fostering clinical reasoning skills.

Next Step...

Last year I implemented a clinical rotation syllabus that emphasized reading peer-reviewed literature on topics such as LBP, shoulder examination, and pain science. This year I will begin incorporating clinical reasoning activity to supplement this knowledge-based curriculum. I'm sure the students will go home with some pretty good brain cramps, but will be better clinicians for it. I know I'll feel better knowing that they got the most out of their rotation at our clinic! I hope you will find this information and the article helpful in guiding your students to become better providers.

An interesting note: I found a more recently published article on clinical reasoning in the PT Journal from 2006 and plan to review it on this blog at a future date. Great stuff!

Jones M (1992). Clinical reasoning in manual therapy Physical Therapy, 72 (12), 875-884

Manual Therapy: What is REALLY going on?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sat, 27 Dec 2008 16:29:00 -0600

Earlier in my PT career I often called B.S. on forms of treatment that didn't seem to pass the smell test. Manual therapists in particular seemed susceptible to jumping on the bandwagons driven by chiropractors (i.e. adjustments, active release therapy, and craniosacral therapy). Not only did I try to avoid any professional association with whom I perceived as quacks, I went out of my way to disprove their methods. As you can imagine, telling someone who believes in Santa Clause "there really isn't a Santa Clause" doesn't always sit well. In fact, it made me downright unpopular with a few folks within our profession.

Being married for ten years has given me some amazing clarity with respect to how I see things. I have come to realize my relationship with my wife would never evolve without intense introspection prior to any external scrutiny I was ready to dish out in her direction. This process has allowed our relationship to blossom into something I could never have dared imagined cultivating on my own. Sitting on my front porch this morning reflecting on our journey, I had another moment of clarity: The evolution of my clinical reasoning and decision-making must precede any relevant criticism of another's.

While I think this process has subconsciously been taking place for a little over a year now, becoming aware of it really had an effect on me. I have been devouring books and peer-reviewed literature in mass quantities. Like my marriage, it has been a transforming journey. More so, the journey makes me realize just how much good work has been done within the fields of movement science. It also motivates me to think we have the opportunity to be a part of the next evolution.

Mechanisms of Manual Therapy

My motivation in writing this post, came from an article in Manual Therapy by Joel Bialosky and associates from the University of Florida. The article provides a framework of manual therapy that has yet to be previously defined to this degree.

Proposed mechanisms for manual therapy vary considerably among our colleagues. A consistent theme however is the identification and correction of biomechanical faults within the musculoskeletal system. This paradigm has been with us for some time and continues to be refined in the peer reviewed literature. However as more evidence emerges, we are discovering there is much more to our manual techniques than correcting upslips and stretching joint capsules.

In an effort to address what "more" there is to our techniques, Bialosky et al provide an elegant proposal of five potential mechanisms at play when our hands are on the patient.

Mechanical Stimuli: Our hands are capable of inducing temporary mechanical changes within connective tissue, but the lasting effects are still uncertain. We have seen positive effects from our manual techniques and assumed a mechanical response to our mechanical technique, but it may not be that simple.

Neurophysiological Mechanism: There is clearly an interaction between the peripheral and central nervous systems during manual therapy. Hypoalgesia and changes in sympathetic activity following joint mobilization technique have been consistently documented in recent literature. Notably the changes in pain threshold and sympathetic activity often occur distant to the site of the manual technique. Something within the patient is clearly interested in what we do!

Peripheral Mechanism: Local tissue injury sets off a cascade of events both near and far within the body. Manual therapy has been recently shown to reduce inflammatory chemicals such as cytokines and substance P along with increasing systemic opioid release. The "good feelings" associated with manual therapy have often been attributed to correction of mechanical faults, but peripheral mechanisms may provide a more reasonable description the therapeutic effect.

Spinal Mechanisms: Renown pain physiotherapist David Butler refers to the spinal cord as an amplifier for sensory modalities. Manual interventions have been recently implicated in modifying both afferent and efferent activity within the spinal column. The bottom line is that the spinal column isn't simply a conduit, but an active participant in determining the effects of manual care.

Supraspinal Mechanisms: Admit it. There have been times where we've thought privately that a condition or response to treatment was "all in the patient's head". Turns out there may be more truth to this statement than we'd previously imagined. Recent animal and human studies implicate specific regions of the brain in mediating the pain experience. Moreover psychosocial factors such as patient expectation and placebo are very likely to affect the outcome of our manual intervention.

Time for Change?
I can't even begin to tell you how sick I am of this word in 2008, but in this case it is appropriate. The moment our hands come in contact with a patient, their nervous system is instantly interested in what's going on. Not only that, but it will play a major role in determining the outcome of the intervention. Once we've gotten used to this idea (and it does take some time), how do we take advantage of it in our treatments? I'd really like to hear your thoughts and am getting excited for 2009!

J BIALOSKY, M BISHOP, D PRICE, M ROBINSON, S GEORGE (2008). The mechanisms of manual therapy in the treatment of musculoskeletal pain: A comprehensive model Manual Therapy DOI: 10.1016/j.math.2008.09.001

Merry Christmas to Everyone

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Wed, 24 Dec 2008 17:41:00 -0600

I'd like to take this opportunity to wish everyone a Merry Christmas. Please enjoy this rendition of Silent Night in the truest spirit of the Christmas season. You may have to double-click it as the embedding feature of my blog isn't always working! Good night and may God bless you all.

Trojan effort...grade five baby!

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 21 Dec 2008 18:29:00 -0600

Early in my career I was very shy about grade five maneuvers in the clinic. I am still very cautious about their use in the cervical spine, and often find thoracic manipulations to be just as useful.

However I felt this demonstration of a lower cervical grade V from our colleagues at USC was worth showing! I particularly like the off-camera "eek!" from the female PT student after the technique.

Nice job Trojans!

Stiff posterior capsule? Maybe not...

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sat, 13 Dec 2008 07:11:00 -0600

It is common practice for physical therapists to include an assessment of the posterior glenohumeral joint capsule in patients with shoulder pain. The rationale is that a tight posterior capsule may exert a "Diablo" effect on the proximal humerus and reducing the subacromial space. This is further substantiated by the obeservaton that GIRD (Glenohumeral Internal Rotation Deficit) often seen in throwing athletes is due to limitations of the posterior capsule. These two clinical observations form the rationale for stretching and mobilizing the posterior joint capsule.

However, there is recent evidence that questions whether the posterior capsule is truly responsible for the limitations in internal rotation commonly seen in our patients. A case report by Poser and Casonato in the Journal of Manual Therapy examined a 42 y/o male with a 12 week history of shoulder pain. This patient was the "classic" impingement case. No cervical pathology was identified and there was no evidence of capsular involvement. The primary findings were positive Hawkins and Yocum's testing along with painful resisted abduction.

Internal rotation was measured using electrogoniometry at 90 degrees of abduction. Additionally, a dynamometer was used to measure abduction force. The patient's pain levels were recorded during the pre-treatment testing. The treatment consisted only of soft tissue massage to the infraspinatus (7 minutes) and teres minor (3 minutes). The patient was positioned in a manner as to avoid any tension placed on the posterior capsule. No other treatments including or activity modifications were given.

After three treatment sessions, internal rotation improved from 68 degrees to 88 degrees and all impingement signs were nearly abolished. The authors concluded that reductions in internal rotation often seen with impingement syndrome may not be attributable to posterior capsular tightness. An alternative theory may be that shoulder pain induces a dysfunction of the posterior glenohumeral muscle musculature.

I must admit am a "mobilizer of the posterior capsule". However after reading this case report and using a bit of reasoning, I realize there may be a better explanation for loss of internal rotation we see in our patients. Although this is but one case report, it certainly made me realize I can never get too comfortable with a particular approach or conclusion. I'm not entirely ready to let go of the possibility that the posterior capsule plays a role in shoulder impingement. However, I imagine with further anatomical and histological of this area will confirm my suspicions that there are other mechanisms at play.

A POSER, O CASONATO (2008). Posterior glenohumeral stiffness: Capsular or muscular problem? A case report Manual Therapy, 13 (2), 165-170 DOI: 10.1016/j.math.2007.07.002

More Neuroscience from the "Ortho Guy"

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Thu, 11 Dec 2008 17:18:00 -0600

Well the semester is finally over. Man I never thought there would be so much to my neuroscience course. It has been an eye opening process that has improved my clinical reasoning and given me a few extra tools in my therapeutic box!

I thought I might take the next few weeks to share some of the topics discussed this semester. On the surface, some of th issues related to neuroscience seem only peripherally related to orthopedic practice. Upon further review, many hit really close to home for many of my patients. I hope you will find them as interesting as I have.

Neuropathic Pain
The mechanisms of peripheral neuropathic pain have been identified more clearly in recent years. Despite the increased understanding, neuropathic pain presents a challenge diagnostically and remains an inadequately treated clinical problem. The current review by Baron outlines evidence to support four likely mechanisms for neuropathic pain followed by a symptom-based classification system. Evidence from both animal and clinical investigations are presented in the review that add strength to the proposed mechanisms. The treatise of the review is that understanding the mechanisms and symptoms of neuropathic pain will provide a clearer path to effectively managing this disorder.

Proposed Mechanisms of Neuropathic Pain
Four potential physiologic mechanisms can explain neuropathic pain. The most peripheral mechanism involves the abnormal sensitization of primary nociceptive (Aδ and C) fibers. A possible mechanism for ectopic firing of primary afferent fibers is an upregulation of sodium ion channels at various points along the axon. Areas of focal upregulation could predispose the neuron to ectopic antidromic and orthodromic impulses. Sensitization of primary fibers has been observed in both animal and human models and is proposed to be a potential cause for heat and mechanical hyperalgesia.

A second mechanism of neuropathic pain is sympathetic sensitization of primary afferent fibers. A normal primary afferent is not sensitive to catecholamines and should not respond to changes in sympathetic activity. However, animal models have demonstrated that injured afferent nerves develop sensitivity to noradrenergic sensitivity. This sympathetic sensitization of the peripheral nerve may take place along the distal branch of the nerve or even at the dorsal ganglion.

The third potential mechanism for neuropathic pain is local inflammation of the periperhal nerve itself. The nerve supply of the peripheral nerve itself is an often underappreciated anatomical an d clinical entity. The nervi nervorum are fine afferent fibers that can communicate noxious activity along the peripheral nerve itself. As such, pain from the nervous connective tissue must also be considered as a potential source for neuropathic pain. As with sympathetic sensitization of the nerve, peripheral nerve inflammation can occur along the distal branch or the dorsal ganglion.

The fourth and final mechanism is central sensitization in the dorsal horn of the spinal cord. Repetitive simulation of primary afferents can result in progressive upregulation of post-synaptic NMDA receptors in the dorsal horn. Under prolonged stimulation, the receptive fields of dorsal horn neurons expand to include Aβ low-threshold mechanoreceptors. This creates potential for mechanoreceptor activity to trigger pain signaling neurons in the dorsal horn; a phenomenon recognized as dynamic mechanical allodynia. Additional mechanisms for mechanical allodynia are proposed including injury-induced C-fiber degeneration and reorganization in the dorsal horn. The mechanisms of central sensitization have been demonstrated in both animal and clinical investigation.

The author utilizes the preceding mechanisms to propose a symptom-based classification system for neuropathic pain to include:

Static mechanical allodynia - gentle static pressure evokes pain
Punctuate mechanical allodynia - normally stinging but not painful stimuli evokes pain (Von Frey hair)
Dynamic mechanical allodynia - gentle moving stimuli at the skin evokes pain
Cold allodynia/hyperalgesia - duh!
Temporal summation - repetitive application of the same painful stimuli worsens symptoms
Sympathetically maintained hyperalgesia - difficult to assess, but improves with sympathetic blockade

These criteria can be used by the clinician to more precisely describe the underlying physiology of the neuropathic event and possibly lead to more effective management strategies.

Clinical Relevance to the Physical Therapist

Traditional symptom-based classification systems have focused on nociceptive or tissue-based models of pain. The present review offers a neurophysiologic dimension to the assessment of the patients’ pain experience. If this classification system can be validated, more specific treatment approaches can be designed. The classification system may have particular relevance for the practicing physical therapist. Physical therapists are able to modulate input, processing, and output paradigms of the human nervous system through movement. As movement involves activation of both ascending and descending pathways, it is likely to have some role in modulating one or more of the mechanisms underlying neuropathic pain.

It is sometimes difficult for me to wrap my head around some of the issues related to pain. However, I've always wondered why a seemingly homogenous population of patients (say post-op TKA) have such varied therapeutic courses. Of course there are the biomechanical factors that are often very intuitive, but there must be something to account for all the variations we see! A better understanding of these mechanisms may help us identify the patients at risk from deteriorating into a more involved pain state and get them back on their feet more quickly.

Baron, R (2000). Peripheral Neuropathic Pain: From Mechanisms to Symptoms Clinical Journal of Pain, 16, 12-20

Problems commenting on my blog?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 7 Dec 2008 09:13:00 -0600

Hey folks. I just discovered that the comments portion of my posts has been deleted. I am working with Blogger to correct the problem. Thank you!

Peripheral nerve function during shoulder arthroplasty

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sat, 6 Dec 2008 16:40:00 -0600

The incidence of peripheral nerve injury during shoulder arthroplasty is reported between one and four percent. However as these numbers are based on retrospective chart review, the actual incidence of intraoperative nerve dysfunction has not been clearly revealed.

The present study utilized intraoperative nerve monitoring to identify the frequency, type, and predisposing factors for peripheral nerve injury during shoulder arthroplasty. Thirty consecutive patients undergoing shoulder arthroplasty participated in this study. Continuous intraoperative nerve monitoring of the brachial plexus was performed by a neurophysiologist. Brachial plexus functioning was monitored by both EMG activity and transcranial electrical motor evoked potentials (MEPs) from six extremity muscles. A significant intraoperative nerve event was defined as a sustained neurotonic EMG activity or a 50 percent reduction in transcranial MEPs from one or more muscles. Both arm and retractor positions were recorded and modified to relieve stress on the brachial plexus when an event took place. If the patient had an intraoperative “nerve alert”, he/she had a follow-up EMG at least four weeks following the surgery.

Seventeen patients had a total of 30 intraoperative nerve alerts. Of the 30 alerts, none returned to baseline with retractor repositioning. However 23 did return to baseline with repositioning of the extremity to a neutral position. Four of the seven patients who did not experience an intraoperative return to baseline MEPs had positive postoperative EMG results. The incidence of nerve dysfunction was associated with a history of prior shoulder surgery and passive external rotation of less than 10° with the arm at the side (P < .05). The authors conclude that intraoperative nerve injury during shoulder arthroplasty is likely greater than reported and certain patients with prior history of shoulder surgery or limited external rotation may be candidates for routine nerve monitoring.
A Great Study

The present study won the 2005 Neer Award from the American Shoulder and Elbow Surgeons. It is a very elegant example of the intersection of neuroscience with orthopedics. Shoulder arthroplasty represents the classic mechanical approach to orthopedic dysfunction. Yet without understanding the neurologic implications of these procedures, we may not fully appreciate the patients’ postoperative courses.

Although the sample size is not overwhelming, 16.7 % of the patients in the study had postoperative EMG changes resulting from an intraoperative neuropraxic event. Interestingly the authors noted that almost half of the nerve alerts occurred within the brachial plexus and not the peripheral nerves themselves. Mechanical strain data indicate the greatest tensile load on the brachial plexus with the arm in 90° of abduction, external rotation, and extension. Intuitively, this makes sense as this is a common intraoperative position for this procedure.

Implications for Physical Therapists

The results of the present study could have implications for the practicing therapist as well. It may be reasonable to assert preoperative improvement of passive ER could reduce the intraoperative traction placed on the brachial plexus. Additionally, the therapists should be aware that in the absence of intraoperative nerve monitoring, there is a possibility that an intraoperative neuropraxic event took place during the procedure. While certainly not something to speculate openly to the patient, it does make a reasonable case for early neural mobilization of the brachial plexus following shoulder arthroplasty in addition to the standard ROM progression.

S NAGDA, K ROGERS, A SESTOKAS, C GETZ, M RAMSEY, D GLASER, G WILLIAMSJR (2007). Neer Award 2005: Peripheral nerve function during shoulder arthroplasty using intraoperative nerve monitoring Journal of Shoulder and Elbow Surgery, 16 (3) DOI: 10.1016/j.jse.2006.01.016

More with less: Conservative management of massive rotator cuff tears

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sat, 6 Dec 2008 16:16:00 -0600

Massive rotator cuff tears within the medically unfit population are a difficult clinical scenario for the medical profession. The nature of the pathology often indicates a surgical intervention, but the procedure is often deemed to be too high risk. The present investigation prospectively assessed 17 patients with massive rotator cuff tears after treatment with an anterior deltoid rehabilitation program. Patients were videotaped attempting active shoulder elevation both before and after the rehabilitation program.

Each patient was given a standardized instruction that involved 12 weeks of daily pendulum exercises and supine active flexion. The protocol was to be performed 3 -5 times daily. As the patient tolerated, they were instructed to gradually increase the resistance of the flexion along with progressively moving to an inclined position. At a minimum follow up of 9 months following the rehabilitation program, the patients were reevaluated. All components of shoulder motion were improved with particular emphasis on forward elevation which improved from 40° at baseline (range 30°-60°) to a mean of 160° at follow up (range 150°-180°). Although seemingly clinically significant, the statistical significance of these findings was not reported. The authors recommend a structured deltoid rehabilitation program for elderly patients with massive rotator cuff repairs.

Massive rotator cuff repairs are clinically challenging even in younger populations. Medically unfit patients with this condition present with even more challenges. While the results of the study speak for themselves, the underlying mechanisms provide some impressive insight into the potential and paradoxical role of the deltoid in normal shoulder elevation. The deltoid has traditionally been thought of as a superior translator of the humeral head within the subacromial space. In the absence of an intact rotator cuff drawing the humeral head inferiorly, augmenting deltoid activity should impair the individual’s ability to comfortably elevate the shoulder. However both this and other recent evidence seriously questions the traditionally-held belief that the deltoid is a humeral head elevator. In fact, a report in Clinical Orthopedics by Gagey found the deltoid to prevent superior migration of the humeral head.

The implications of these findings are significant to say the least. First and foremost, if massive rotator cuff tears can be effectively rehabilitated in the medically unfit population, what about the medically fit population? Would this not make the case for a retooling of our current approach to conservative management of rotator cuff pathology prior to considering surgical intervention?

Secondly, as clinicians we are traditionally cautioned against “biasing the deltoid” during active shoulder movements in the presence of rotator cuff pathology. The present investigation provides further evidence against the notion that feed forward biasing of selected muscles may not be necessary to achieve a significant functional improvement. In fact, in this case the patients were only given verbal instruction to follow a written protocol and given no specific feedback regarding their performance of the activity. Again the implication is that the patient’s inherent feedback mechanisms were sufficient to perform and progress the activities.

This fairly straightforward study is not without limitations, but the implications for our daily practice are important. Therapists should be increasingly aware that patients can achieve significant improvements in motor control and function in the presence of severe mechanical impairments, and that these improvements can occur without micromanagement of specific movement patterns as traditionally outlined. This doesn’t negate the potential role of the therapist in the rehabilitative process, but it should raise questions as to the exact nature of our role in our patient’s recovery of this condition.

O LEVY, H MULLETT, S ROBERTS, S COPELAND (2008). The role of anterior deltoid reeducation in patients with massive irreparable degenerative rotator cuff tears Journal of Shoulder and Elbow Surgery, 17 (6), 863-870 DOI: 10.1016/j.jse.2008.04.005

Lubbock and Legacies

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Mon, 10 Nov 2008 20:36:00 -0600

I just got back from my most recent trip to Lubbock, TX. The atmosphere in that west Texas town was electric as the Red Raiders took another step toward a potential national championship in football. As a Longhorn (whose team lost to Tech the previous week) I was really impressed with the enthusiasm and passion of this town for its team.

The purpose for my visit was to attend the contact session for my Neuroscience in Orthopedics course. As with many of this year's adventures, it was another eye-opening experience. When I set out this year to improve my understanding and clinical reasoning, I had no idea just how much I'd learn or how many great people I'd meet.

We spent the entire weekend exploring topics ranging from receptor biochemistry, peripheral and central sensitization, neuropathic pain, and a variety of other issues related to the assessment and treatment of painful conditions. The material was engaging and prompted a number of great clinical stories from my classmates. My laptop left the session about 200 megs heavier with journal articles. Interestingly, not even one of them included a clinical prediction rule!

One of the most truly humbling features of my trip was the opportunity to meet several fascinating members of our physical therapy community and the field of medicine. I briefly met one of the founding members of the World Institute of Pain, anesthesiologist Gabor Racz, MD. The interaction was brief, but it was great to talk with someone who has contributed so much to the field of pain science. I also had a chance to meet clinician and author Omer Matthijs. His hard work and clinical experience continue to set the right kind of examples for our profession. While the classroom experiences I had were memorable and continue to evolve my clinical reasoning, the fellowship with my peers and instructors made an even more lasting impact.

One of the talks led by our professor Phil Sizer drifted somehow into a brief but powerful mention of the legacy we all leave within our profession. In light of my encounters with Dr. Racz and Omer Matthijs, this tangent really resonated with me. It got my mind going, and I began thinking of the legacy I might leave behind. I also turned my attention to the legacies many of our peers are creating and I was hit with a sense of optimism for our profession.

It has been nearly a year since starting this blog and it has already been a transforming experience for me. I truly appreciate your joining me on this journey and hope it, in some way, inspires you to reflect on the legacy you may be creating. It is my sincerest hope our collective efforts within the profession will continue to carry the torch for those who have worked so hard to light it. Until next time!

Electrotherapy on the Web

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Sun, 12 Oct 2008 20:35:00 -0500

Modalities have become the poor cousin for many outpatient physical therapists. Myself included. We often look down upon that ultrasound or TENS unit because it isn't "evidence-based" or doesn't involve the latest CPR-derived manual technique / exercise. Despite this sentiment shared by many therapists, the use of therapeutic modalities persists in most outpatient centers. This had me wondering: Where is the latest evidence on electrical modalities in physical therapy? In searching for my answer, I stumbled on a very useful website.

Electrotherapy On the Web

This is a website is run by professor and physiotherapist Tim Watson of the University of Hertfordshire in the U.K. The website includes a surprising number of useful links and guidelines for the use of electrotherapeutic modalities. Professor Watson includes a number of easily downloadable resources for the practicing physical therapist. If you utilize electrotherapy in any capacity or are simply wanting to learn more, I strongly suggest a visit.

I don't know how much more I will be using electrotherapy in the clinic, but I can say this website will assist in making better decisions regarding their use. Enjoy!

Cutting or bleeding edge?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Mon, 29 Sep 2008 21:41:00 -0500

Hurricane Ike came and went, but it almost feels like he's still hanging around the Gulf Coast. The devastation was truly remarkable particularly for places like Galveston and the Bolivar Peninsula. If you've never been through a good sized hurricane, I wouldn't recommend it. My Alma mater, UTMB - Galveston, is finally getting back on its feet, seeing patients, and teaching PT students again. My thoughts are with them and any other folks devastated by this storm. We finally got the lights turned on and life is returning to normal, which for me means getting back to blogging on a more regular basis. The clinic has never been busier so there is definitely plenty to talk about.

For a self-proclaimed "ortho-guy" I certainly have been immersed in a great deal of neuroscience this year. I had a brief yet spirited set of interactions with the folks on SomaSimple, and currently enrolled in a class titled "Neurosciences in Orthopedics" at Texas Tech. I have to admit the study of neuroscience is really filling in a lot of gaps in my understanding of orthopedic conditions.

Neuroscience is creating some very novel therapeutic inventions. The paradigms of neuroscience are building on theories such as David Butler and Lorimer Moseley's work on pain as well as Michael Shacklock's neurodynamics. The exploration of neuroscience arises from an understanding that traditional orthopedic paradigms aren't always hitting the therapeutic bullseye. For example what explains the persistent symptoms of lateral epicondylalgia or anterior knee pain? These conditions often defy objective diagnositic testing and treatments based on the traditional tissue-healing inflammatory model. I would encourage anyone interested in learning more about these approaches to visit the sites listed above.

As with any treatment approach, I remain cautiously optimistic. As my father, a practicing family physician and medical veteran, often cautions me: It's good to be on the cutting edge, but avoid getting caught on the bleeding edge. New and different aren't synonymous with correct and irrefutable. We must continue to develop our understanding of human function without strictly adhering to old paradigms. At the same time, we must be prepared to embrace emerging theory without getting caught-up in the latest fad. At the end of the day, sound theory supported by strong evidence will continue to guide the best practitioners of this profession. I believe the field of neuroscience will meet the test of both theory and evidence and continue to provide salient answers.

One final note, I hope to make more regular contributions to my blog and appreciate everyone hanging in there with me. I'm in the midst of balancing my contributions to this blog with teaching, studying, treating, and recovering from coastal natural disasters! As this semester rolls on, I hope to contribute more regularly. Thanks and have a great weekend!

Calcaneal and Plantar Nerves: Overlooked contributors to heel pain syndromes?

roderickmpt@embarqmail.com (Roderick Henderson, PT, OCS, CSCS) — Wed, 10 Sep 2008 20:40:00 -0500

So I'm sitting here in my living room watching coverage of the latest impending apocalypse (Hurricane Ike) churn in the Gulf. You might think it's an odd time for this Gulf Coast native to be thinking about heel pain, but here I am...thinking about heel pain. We can discuss the reasons I have no life at a later date.

Diagnoses seem to come in spurts in this clinic and I've recently been referred several cases of both infracalcaneal and retrocalcaneal heel pain. As with many of my treatment approaches, my tactics regarding heel pain have evolved considerably over the years. Despite this ongoing refinement, I still find heel pain to be both fascinating and frustrating clinical entity. For me, it is the LBP of the foot.

I recently did a literature search on the various incarnations of heel pain and was relieved to find I'm not the only one out there navigating through the fog. There are still gaping holes in our knowledge and understanding of this condition. In the midst of my literature search, one article stood out enough that I felt it worth mentioning.

Overview and Methods

The article was published in 2003 in the Journal of Foot and Ankle Surgery. The authors set out to determine if sensory abnormalities existed in the medial and lateral calcaneal nerve distribution in patients suffering from plantar heel pain. The study examined 97 feet in 82 patients reporting symptoms consistent with plantar fasciits including poststatic dyskinesia and tenderness to palpation along the medial calcalneal tubercle. Patients were excluded from the study if they had comorbidities such as radiculopathy or an equinus foot. Neurosensory testing was performed using a pressure-specified sensory device used to detect compression or entrapment of both large and small nerves.

Results and Conclusions

The authors found a significant number of patients with plantar heel pain display abnormal sensibility within the branches of the posterior tibial nerve. Abnormal sensibility was noted particularly within the medial calcaneal nerve (P<.0008) and lateral calcaneal nerve (P<.0001).

It is our belief that entrapment of the MCN plays an important role the development of plantar heel pain, and we were able to quantify abnormal sensibility in the cutaneous distribution of both the MCN and/or the MPN in a significant number of patients with plantar heel pain. The observed nerve dysfunction is most likely secondary to entrapment of the nerve trunk, or trunks, as a result of repetitive mechanical irritation. In response to this pathologic stimulus, we hypothesize that the injured nerve trunk undergoes in-continuity fiber disruption and intra- and perineural fibroplasia. Because 49.48% of our patients displayed abnormal sensibility in the cutaneous distribution of both the MCN and MPN, a proximal neural origin such as proximal tarsal tunnel entrapment of the PTN, or even lumbosacral radiculitis, plexopathy, or sciatic nerve impingement, should be considered in these patients.

Clinical Implications?

A treatment theme that seemed to resonate with me in this article was that of regional interdependence. For example, two of my patients with heel pain also have persistent lumbar pain - one with motor radiculopathy ipsilateral to the heel pain. These comorbidities may play more of a role in distal pathology than previously appreciated. Secondly, the findings of this article could lend support to the notion that neurodynamic movements such as lower extremity nerve gliding could play a role in more distal conditions such as heel pain. In addition to our traditional mechanically-based therapeutic regimen, it may make practical sense to consider structures such as the peripheral neural tree as possible contributors to the patient's problem.

Here's hoping all my neighbors along the Gulf Coast stay dry this weekend!

Rose JD, Malay DS, Sorrento DL (2003). Neurosensory Testing of the Medial Calcaneal and Medial Plantar Nerves in Patients With Plantar Heel Pain The Journal of Foot and Ankle Surgery, 42 (4), 173-177