Are you an expert clinician?

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?

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

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!

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...

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"

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?

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

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

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