Much depends on who one reads, and when, but the generally accepted incidence of rotator cuff tears, partial or full, loiters around 20% in the general population. Typically, the cuff muscles elect the supraspinatus to bear the injury. It should be noted that, interestingly, a sizable percentage of supraspinatus lesions are intratendinous, as opposed to bursal- or articular-sided in description. Of further interest may be that the supraspinatus muscle hosts five distinct layers, each with unique characteristics; weaving arterioles, loose connective tissue, varied axes of angled collagen bundles and all.

Enter Tanaka et al. Once a rotator cuff tear is apparent, the success rate of conservative treatment varies from 33% to 88%, they cite. This range should raise the antennae of suspicion in any clinician. Surely superior categorization exists so as to better predict successes. Tanaka et al., having measured and weighed, came up with the proceeding list in a recent publication. The four factors that correlated very well with a successful outcome following conservative treatment include 1) a preserved range of motion in external rotation (>52 degrees), 2) negative impingement signs, 3) little or no atrophy of the supraspinatus muscle, and 4) preserved intramuscular tendon of the supraspinatus. Patients showing at least three of these four factors theoretically enjoy success following conservative management 87% of the time. Obviously, unless one keeps some extraordinary physical examination skill or special test, the existence of which I am unaware, advanced imaging is prerequisite in determining the above listed fourth factor.

Follow this thread to read the article in its entirety on Pubmed (free PMC article).

Introduction

Inside the walls of a hospital building, or anywhere, really, continuous passive motion (CPM) machines generate unusually dull conversation. Yes, most members of the allied health team are familiar with the apparatus, but few dwell on them. Few really think about them. The gears of each machine simply drone on in perpetuity and patiently trace their arc. And the lambswool kit that lines the frame of the machine invariably mats itself slick and is corrupted. The device is manufactured in all shapes and sizes and for many joints. CPM, however, cannot be defined simply within the confines of a motorized device. Rather, it is not contained and bubbles over and spreads to describe a concept, far from dull.^26-29 How, then, to learn this concept? Well, a good linguist will hail context as king. Whether learning a single word or a string of words, both individual meaning and collective understanding are best realized only upon inspection of the native context in which they were left. Vary too far from or blunder too close to this context and the messages are obscured and rendered inaccurate. Forty years have past since the inception of the original concept of continuous passive motion and have been somewhat diluting. The objectives of this review are several. Historical context will be built to better understand and therefore grasp the significance of CPM. Relevant basic science principles will be reviewed, particularly the inflammatory response, the pathophysiology of joint stiffness, and the biological phases of normal cartilage maturation following insult. Indications for application will be delineated and then considered using the best available evidence drawn from primary literature, clinical reasoning, and logic. Finally, recommendations for application and unfolding, prospective research will be discussed.

Body 1: An Historical Perspective

Strict, undisturbed rest best manages musculoskeletal disorders and injuries. To disturb the rest is to disturb the healing, and proportionately, claimed the vast majority, if not all, medical practitioners over the past several centuries. Many early sketches and writings even suggest that immobilization to treat injury traces easily back to Hippocrates (460-337 BC) and even extends to ancient Egyptian civilization. Considered the father of orthopaedic surgery in the English-speaking world, Hugh Owen Thomas (1834-1891) strongly advocated rest and taught that immobilization must be “complete, prolonged, uninterrupted, and enforced; and that an overdose of rest was impossible.”^{5, 12, 21-24} His language led but also reflected the predominant thinking. Several late nineteenth century physicians, however, began to wade against these practices. Julius Wolff (1836-1902) described that bones in fact remodel in accordance with repetitive loading and Just Lucas-Championniere (1843-1913) taught that movement hastened healing and actually benefited injured tissues.⁵

In 1933, Ely and Mensor discovered histological evidence of thinning and fibrillation of the articular cartilage in the ankle joints of dogs consequent to immobilization. Seventeen years later, Salter and Field showed that immobilized joints in humans were similarly damaged and went on to hypothesize that this would be associated with continuous compression of the opposed joint surfaces that were deprived of synovial fluid nutrition.^{1, 9, 15, 28} Curious, the team investigated the question further. They discovered that 8 days of either a compression clamp across or the immobilization of a rabbit joint, the articular cartilage contact areas necrotized into an irreversible lesion that they called “compression necrosis of articular cartilage”²⁸ In 1965, Salter et al noticed that 3 weeks of prolonged knee immobilization yielded similar results; the synovial membranes adhered to the underlying articular cartilage and were irreversibly degenerated. These observed lesions were called “obliterative degenerations of articular cartilage.”¹⁵ Quite concurrently, data from various research groups began to advise that exercise and intermittent active motion, that is, repetitive articular cartilage loading and unloading, actually stimulated joint nutrition!^{13, 14, 15, 25} Thus and with building momentum, Robert B. Salter, the Canadian paediatric physician and basic scientist, began to induce general biological principles from these and other specific fragments of observed empirical data. Previous to these decades of research, medical reasoning had been largely based on deductive logic, where a specific conclusion is drawn by inference out of that which is general.

A scientist is always asking questions and, ultimately, Salter was in pursuit of the centuries-old variety. Does articular cartilage possess the capability to heal in measurable and meaningful ways? Additionally, Salter wanted to afford biological alternatives to prosthetic joint replacement for irreversibly destroyed arthritic joints. Noticing the patterns of rest and motion, he devised a more focused series of small animal basic science experiments. He discovered that neither immobilization nor intermittent active motion served to appropriately stimulate the healing of full-thickness articular cartilage defects. After no less than 8 years of time and no fewer than 23 experimental and clinical observations, Salter conceived continuous passive motion for the treatment of musculoskeletal disease or injury, specifically synovial joint lesions. Salter engaged his colleagues in the Department of Mechanical Engineering at the University of Toronto and John Saringer, a professional engineer in 1978. The collaboration yielded the continuous passive motion device, a machine to bridge the theoretical and the actual.^{15, 26-29}

Body 2: The Basic Science

CPM intervenes broadly across medical practice. In addition to demonstrating excellent potential for the healing and regeneration of articular cartilage, CPM is very typically used to prevent arthrofibrosis subsequent to joint trauma, surgery or disease. Biological tissues adhere to relatively predictable patterns of healing following insult. Differences in anatomical arrangement and physiological function across tissue types dictate response variations. Synovial joints, uniquely, present an interesting study secondary to their conglomerate structure, skeletal, articular, bony, and dense fibrous tissue all interacting. And because continuous passive motion has been applied predominantly towards synovial joints, to establish what should occur in health and following injury is to best judge change. O’Driscoll and Giori synthesize relevant data and explore the pathophysiology of joint stiffness, organized into four stages.¹⁸

Bleeding initiates the first stage and occurs within minutes to hours in response to trauma, whether surgical and controlled or inadvertent and uncontrolled. While not atypical for bleeding to ensue following the application of trauma to most biological tissue, the joint is provoked uniquely. The introduction of blood into this enclosed system instigates increased intra-articular pressure, which tends to distend the joint capsule and swell the periarticular tissues. With pressure elevated, the joint seeks relief through an attitude of flexion or extension towards maximum potential volume. Once maximum intra-articular volume is arranged, the capsular distension decreases and both rest and attempted deviatory movements generate less pain. The maximum capacity of the joint capsule for the knee has been demonstrated to be approximately 35° of flexion and the elbow 80° of flexion.¹⁸ The natural tendency to drift into flexion and away from pain considered in concert with autogenic reciprocal inhibition of the primary joint extensors helps explain why extension is so difficult to achieve following trauma.^{18, 23} The second stage is driven principally by osmotic behavior over hours to days and is termed edema. When blood accumulates inside a joint, inflammatory mediators are released by platelets and solute builds. Local vasculature dilate and their solvent, primarily plasma, is dispersed among the solute. Periarticular tissues swell and become more resistant to change, in particular change away from the position of maximum volume. Next, over days to weeks, the edematous articular and periarticular tissues are infiltrated by granulation tissue in the stead of fluid. This process marks the beginning of extracellular matrix deposition and the third stage of stiffness. Lastly, the adolescent granulation tissue matures and invents a scar. The scar is dense and fibrous and comprised predominantly of type I collagen, which resists tensile stress very well, a feature not overly desirable in a moving part.¹⁸ These are the stages that represent the pathophysiology of stiffness, in general.

In addition to a working knowledge of pathophysiological trajectories, sound scientific reasoning obliges the astute clinician to also carry specific processes. Articular cartilage lesions being a top target of current research and a major impetus for the conception of CPM, the biological phases of cartilage maturation following trauma and repair are discussed. While several discrete reparatory procedures exist, for simplicity, subchondral bone microfracture will be used as a model. These biological phases follow the general principles of tissue healing, but with some distinctives. The first phase is called the proliferation phase and is the most delicate. Here, the healing cartilage works to rouse specific cells that will produce matrix specific markers.3, ^{10, 20, 22, 30} Typically, 4 to 6 weeks of vigilance are required. The next, transitional, phase intermingles with the activities of the proliferation phase and may begin as early as week 4 and last through week 12. Regard must be paid to the movement quality of the periarticular tissue as the fragile articular cartilage begins to strengthen. Controlled and repetitive loading and unloading of the joint employs synovial fluid nutrition and mechanical stimuli to persuade maturation on. From week 12 to month 6 the tissue remodels further, organizing to grow stronger and more resilient. Great stress is now required to disorganize the tissue. Finally, month 15 to 18 see the cartilage reach its full maturity, where the lesion site displays histological and biomechanical behavioral properties most reminiscent of the native tissue.^{3, 30}

Body 3: Indications and Outcomes

Salter originally described 13 experimental CPM models, which included full-thickness defects, autogenic osteoperiosteal grafts in major defects, free autogenic periosteal grafts, and periosteal allografts.²⁶ This group has been largely substantiated by others.^{5, 16, 18} But in 1982, when Coutts et al evaluated the effect of continuous passive motion following total knee arthroplasty (TKA) and found favor in the results, the concept of CPM, reflected both in subsequent randomized controlled trial design and also in general thinking, was pigeonholed to enjoy fewer indications.⁸ A multitude of successive studies have evaluated the effect CPM following TKA and discovered or rediscovered analogous information. Namely, across varied conditions, CPM yields favorable short-term range of motion (ROM) results, but no beneficial long term ROM or functional outcomes.^{2, 7, 11, 14, 21} A recent Cochrane database systematic review concurs and decides that the long-term effects of CPM on TKA are equivocal.¹¹ Proponents of CPM, however, argue that experiments have been carried out improperly. The motion arcs are usually too small and the time too sparse, they rejoin.^{4, 18, 26} CPM applied to TKA tends to shorten length of hospital stay, improve active knee flexion, decrease analgesic requirement and manipulation under anesthesia, and save monies.²⁶

One must not forget that total joint arthroplasty represents a particular joint intervention from a singular approach. And where arthroplasties obviously preclude the possibility of native articular cartilage recovery, CPM predicts successes. In fact, as discussed earlier, Salter originally devised CPM with articular cartilage healing in mind. Perhaps greater efficacy is found here. In 1983, O’Driscoll and Salter presented that CPM both effectively cleared hemarthrosis from a synovial joint and also stirred neochondrogenesis in free intra-articular periosteal autografts in rabbit hind limbs.^{18, 19} Rodrigo, Frisbie, Reinhold, and Wilk, alongside collaborators, have each justified more recently the successful role that CPM holds when applied in concert with prevailing articular cartilage procedures.^{3, 10, 20, 22, 24, 29, 30} Further and more specifically, Nugent-Derfus et al. have recently shown that CPM delegates mechanical stimuli in vivo which stimulate chondrocyte PRG4 metabolism, a putative lubricating and chondroprotective molecule.¹⁷ The future marriage of CPM to articular cartilage procedures remains under study. Perhaps the “impossible dream” of cartilage healing is now less incorrigible.¹⁵

Discussion & Reasoning

In 1986, Salter wrote, “ despite the fact that rest and motion have always been two of the most commonly prescribed methods of management of diseased and injured musculoskeletal tissues, their indications, duration, and therapeutic value remain controversial.²⁷ Continuous passive motion defines more than an adjective to describe an external motorized device. The concept emerged during an era still hesitant to allege that strict immobilization was not the best practice for a diseased or damaged synovial joint. Shortly after conception, CPM was seemingly pigeonholed to enjoy fewer indications and understanding focused on its platitudes. While a wide range of recent primary literature has been elucidated, numbers alone have weak minds: they can easily be persuaded to say most anything. CPM is recommended only after thorough reasoning, which employs basic science⁶, unique pathophysiology, clinical reasoning, and, most importantly, patient milieu and goals. The World Health Organization (WHO) defines disability as a complex term that swathes impairments, activity limitations, and participation restrictions. CPM alone cannot address disability beyond the impairment level and, thus, must necessarily coordinate with other disciplines to achieve full rehabilitation.

To read John’s article in PT Products Online click here

CPM References

The knee can practice certain positions that really torment its ligamentous restraints. And there is perhaps no more famous a checker of knee attitude than the anterior cruciate ligament (ACL). Famous because sometimes it sprains or ruptures while loyally checking. In The New York Times Well column, Gretchen Reynolds produces some interesting concepts relevant to ACL health. Reynolds asks “are bad knees in our genes” and cites a recent article that was published in The British Journal of Sports Medicine that answers “somewhat.” In said article, researchers studied families with funny patterns of ligamentous knee injury; funny “peculiar” and not funny “ha-ha”, that is. They found within these groups, two sets of twins and one set of triplets, each had torn their ACL! Peculiar, indeed. Scientists at the University of Capetown in South Africa enjoy this because they claim to have isolated a gene that predicts ACL tears. Genetic research and twin studies always create logic bridges between one another. The at fault gene is purported to transcribe collagen whose properties do not resist change well and may tear more easily.

So, what question do these data answer and what are the implications? Well, as previously stated, certain movements really torment the ligamentous restraints of the knee; period. The introduction of genetic collagen disorders into this conversation simply describes more precisely how the ligament may respond to strain. A healthy ligament could theoretically tear at any time given the appropriate environmental conditions. A person with the “ACL gene”, then, is necessarily condemned to sustain a rupture? Not hardly. Conservative management can yet still train the knee to avoid positions of high ligamentous stress. Given two identical persons, one with and one without robust collagen, shown the same knee stress, then, yes of course, one knee would be at a higher risk of ligamentous injury.

Risk factors pose questions of spectrum and degree. Reynolds’ article introduces another measurement by which scientists are ranking ACL risk factors along another spectrum. The nature versus nuture debate rages on and risk is almost certainly still best thought of as a combination of intrinsic, extrinsic, and environmental factors, utterly unique to each person.

Jane Brody, in The New York Times Health, recently reviewed the health benefits of Tai Chi, which, in like manner to yoga, describes a string of movements that accrue and form a system. The system, then, guides its practicioners into a certain routine and subsequently better health. Brody makes clear the importance of learning the system from a qualified instructor. In general, the movements drawn by the joints are light and energy cost manageable in Tai Chi. And the primary literature evidence suggests that some very real health benefits wait. Decreased blood pressure and increased balance, to name two of many. As the inquiry of the scientific community continues to yield data, many systems of antiquity are found to be quite favorable. To learn more, let Brody finish her story here.

Exercise ball chairs. You know them. You know them well. In fact, you know someone who uses one; they sit right next to you at work. Sometimes they get up too abruptly and the ball drifts into your leg and creates a small static electricity reaction, which distracts the pant leg and your attention, in that order. But is the exercise ball chair a good idea? What does it really do? Anahad O’Connor, in New York Times Health, discusses. Conflicting data exist on the efficacy of sitting on an exercise ball as opposed to a traditional, pseudo-ergonomic chair. A 2009 British study found that exercise balls produce similar amounts of “slumping,” while a Dutch study of the same year found that they facilitated greater “trunk motion.” Hmmm…so which is it? Well, just think about it. The rigidity of a standard office chair restricts slumping more stringently than a pliable exercise ball would. The potential for slump on the exercise ball is thus greater and more catastrophic when it occurs than on a standard chair. Conversely, the pliability of the exercise ball challenges the muscles of the trunk in a way that the standard chair simply never could. But the benefits of this challenge take active, cognizant work. Sitting on an unstable surface probably enables precipitous change, therefore, in general and in either direction. So, through a risk-benefit frame, the exercise ball may be viewed as more “risky” but also more “rewarding” if properly employed. Check out the full article to learn more.

Goals drive, draw, determine, and, sometimes, drag us forward. But forward we will go when an appropriate goal has been written. In the New York Times Fitness & Nutrition section, Gina Kolata describes her goals, the bike race that ensued, and the lessons she and her husband gained from the experience. Quite interesting and motivating. Two famous Ivy League University studies enjoy Gina’s article. First in 1953 and then again in 1979, these two studies of similar construction found that clearly defined goals, particularly those that are written, succeed much more commonly than those that are vague. Learning a new sport, skill, or improving upon an existing one, is most effectively realized with small, reasonable and clear goals. Check out the article in its entirety to learn more!