A Clinical Framework Utilizing a Precision Approach

A Clinical Framework Utilizing a Precision Approach

Craig Liebenson

Laura Latham

Jae June Rhee

Gerissen Tang

Ryan Chow

Chad Buohl

General Considerations


Low back pain (LBP) is a common problem. Chronic LBP is a leading source of worldwide disability and a cause of staggering health care costs. According to a recent World Health Organization (WHO) bulletin authored by Traeger et al,1 it “is the single biggest cause of years lived with disability (YLD) worldwide,2 and a major challenge to international health systems.” The traditional biomedical model is incomplete and has led to poor management of the LBP patient. In fact, Traeger et al1 state there is strong evidence that unnecessary care, “including complex pain medications, spinal imaging tests, spinal injections, hospitalization and surgical procedures, is hazardous for most patients with low back pain.”3,4,5

We need to update the biopsychosocial (BPS) approach considering the multitude of factors that make up the patient experience. Because pain is multifactorial, rather than focus on a single cause of pain, it is better to acknowledge the complex systems at play and develop an agile approach to handling uncertainty.

Given the multifactorial nature of the LBP problem, a question posed by a multidisciplinary group of experts is “what potential is there for identification of individual biomechanical factors to play a role in treatment of LBP?”6 They state, “Our numerical and analytical simulations of multifactorial presentation of LBP demonstrated that if a large number of factors contribute to an individual’s LBP, any treatment strategy that seeks and treats the most dominant factor is less effective than treating any 2 or more factors chosen arbitrarily.7 Furthermore, the probability of identifying sub-groups, that might respond favorably to a specific intervention in such a population, tends to zero as the number of factors increases.”

The challenge of LBP is the difficulty in confirming either the specific pain generator or source of biomechanical overload in the kinetic chain.8 Thus, most LBP is reluctantly considered to be nonspecific.9 This does NOT mean there is no cause, only that LBP has a complex etiology with multiple pain sources and perpetuating factors.9,10,11

In spite of this limitation, a diagnostic triage can still be performed. Diagnostic triage is a scientifically proven approach that classifies pain sources in the following way (see Chapter 3):

Red Flags—approximately 1%

Nerve Root—approximately 10%

Nonspecific LBP—85% to 90%

Although the ability to provide a specific diagnosis is limited, an outcome-based approach benefits from screening for yellow flags (YFs), which are risk factors of chronicity3,4,5 (see Chapter 7). Patients with either nerve root or nonspecific LBP with YFs benefit from a cognitive-behavioral (CB) approach (see Chapter 16).8 CB education, therapy, or training focuses on
affective (i.e., emotional) or cognitive (i.e., beliefs and behaviors) factors (see Chapters 13 and 16).12 The goal is to screen and intervene in a person-centered way in order to reduce threat of pain or reinjury and enhance self-efficacy.8,12

Taking a thorough history is an essential first step in creating the patient profile (see Chapter 37). This idea is nothing new, but has been underestimated and underutilized in previous models. Understanding the patient’s story, creating a therapeutic alliance, and inspiring the patient to take an active role in care rather than being a passive recipient is the cornerstone of this approach. The clinician should be able to gather information about the patient’s goals, fears, worries, beliefs, and concerns, as well as activity intolerances (AIs). All patients require a diagnostic triage to rule out red flags of serious disease. Although necessary, this is not sufficient to properly manage the case. It is also essential to identify the patient’s YFs indicative of a poor prognosis. Finally, the clinician should establish baselines for a patient-centered rehabilitation by identifying the patient’s current capacity, required capacity, and demands.

Patients with nonspecific LBP should be reassured that they don’t have red flags, a nerve root problem, and given functional reactivation advice consistent with CB principles.3,4,5 Commonly, it is believed that such advice ignores the person’s pain or suffering. In fact, properly administered patient education explicitly creates therapeutic alliance and provides reassurance (see Chapters 13 and 16).

A novel strategy that recognizes the heterogeneity of patients utilizes the Pain Mechanism Classification System (PMCS) (see Chapter 9). The PMCS’ appreciation of the role that psychosocial aspects play in the pain experience means that clinicians need to develop a skill set that reflects the ability to assess and manage pain mechanisms that are influenced by psychosocial as well as biologic factors.

The physical examination including orthopedic examination, neurologic examination, and movement assessment is utilized to gather further information about the patient’s mechanical sensitivities (MSs), painless dysfunctions, and current capacity. In musculoskeletal care for the individual in pain, goal setting and outcome measures play a critical role in allowing practitioners the evaluative tools to demonstrate change to patients and third-party payers.

When the painless dysfunction that is nested to the chief complaint has been identified, the clinician can begin to guide the patient through movement prep (MP) targeting this weakest link. During movement, pain is monitored but not feared. Teaching the patient that every hurt does not equal harm is a key lesson the clinician can provide to allow for the individual to have a positive experience with movement. The clinician guides the patient through movements when there is some pain (<3/10), using caution during movements with moderate pain (4-5/10), and changing the exercise when there is pain (more than a 5/10; see Chapters 9, 37, and 38). The MP gives way to training general physical preparation (GPP), working the fundamental movements of squat, hinge, single leg bias (e.g., lunge), push, pull, and locomotion (e.g., carry). Understanding that every exercise is a test allows the clinician to constantly be auditing to find the hardest thing the patient does well.

Proper load management is important in building the robustness and resiliency necessary to ensure that capacity is greater than demand. Using a constraints-based approach, consistent with Dynamic Systems Theory (DST), varying the task and environment creates an opportunity to develop adaptability in the individual so they will be able to respond to unpredictable stress and become antifragile.

To this point, the approach has been entirely active. This creates autonomy and independence for the patient and in many ways is essential to the updated paradigm. Although manual therapy is not lost, it should be limited to an as-needed basis to enhance recovery and reduce delayed-onset muscle soreness. Whenever possible, manual therapy, modalities, medications, and injections should be utilized only if MP and GPP are poorly tolerated and when CB is occurring simultaneously.

The solution is to realize that there are general principles that can highlight a path toward “pattern recognition” or the precision necessary for offering patient-centered or individualized care pathway. Principles also allow health care practitioners (HCPs) to insert whatever skills and tools they know now and integrate others in the future, thus enhancing all current and future tools. The four principles outlined in Chapter 38 allow the HCP to be both evidence based in general and agile enough to personalize a precision approach.

Personalizing a Precision Approach to Nonspecific LBP

Each patient needs

  • Reassuring advice regarding the integrity of the spine (i.e., false-positive imaging results), safety of resuming activity, and that not all hurt equals harm.

  • Reactivation advice about how to perform basic movement patterns (i.e., squat, single leg bias, hinge) with acceptable form as it relates to their chief complaint.

  • Resilience to handle the demands of their lifestyle. Thus, strength (resistance) training is essential to build sufficient robustness.

  • Variability of training to prepare for random, unexpected life challenges.

Figure 39.1 Percentage of children meeting PA guidelines in Australia. Adapted from Figure 2, Australia AHK. Physical Literacy: Do Our Kids Have All the Tools? 2016 Report Card on Physical Activity for Children and Young People. Adelaide, Australia: Active Healthy Kids; 2016.

This framework allows for a step-by-step efficient process that can be applied to any patient to bridge the gap from what they have (capacity) to what they need (demands). Rehabilitation is a time-consuming process and thin slicing is needed, otherwise patients will not stay engaged long enough to get the results they want and need. The rehabilitation prescription, rather than being a protocol based on pathology or symptoms, is a precision process following economical yet potent principles.

A General Approach to Rehabilitation for Activity Limiting Musculoskeletal Pain


  • The problem—disability epidemic

  • The trigger—mismanagement of persistent or severe pain

  • The fuel—inactivity

  • The solution—address overprotection and underpreparation

The main problem is accentuated by the fact that by the time a child is 4 years old, there is only a 50% likelihood they are meeting internationally recognized activity guidelines!13 (see Fig. 39.1).

Solution—train like an infant—explore options through play.

Therefore, in our assessment we use health span tests appropriate for different stages in life:

Overall goal: be like a forager or hunter/gatherer by limiting prolonged sitting and engaging in regular, moderate-vigorous intensity physical activity.

How Is Reassurance Given?

  • Magnetic resonance imaging (MRI) is not the whole story (see Fig. 3.6)

  • Activity is safe

  • Load monitoring scale (see Chapter 37)14

Figure 39.2A One-leg standing test. Positive Trendelenburg sign. Lateral shift and oblique position of the pelvis, contralateral shoulders elevated.

Figure 39.2B Lunge test.

Figure 39.3A 2 leg squat.

Figure 39.3B 1 leg squat.

Figure 39.4 Example of gluteal activation test—2 leg gluteal bridge.

Figure 39.5 Example of hip mobility test—shinbox.

Figure 39.6 Example of squat—goblet squat.

Figure 39.7 Example of lunge—slider reverse lunge.

Figure 39.8 Example of push—bench press.

Figure 39.9A Example of pull—cable pull start position.

Figure 39.9B Example of pull—cable pull finish position.

Figure 39.10A Example of hinge—single leg Romanian deadlift (RDL), start position.

Figure 39.10B Example of hinge—single leg RDL, finish position.

Figure 39.11 Example of carry—front rack kettlebell carry, bottoms up position.

A Measurable, Outcome-Based Approach to Implementing the Four Principles

According to Dan Pfaff, “it’s about landmarks not timelines.” So we give people hope by finding reversible functional pathologies that give people both hope and an achievable plan. This is done to help them become more PREPARED because “it’s not the activity that’s harmful but the activity you’re not prepared for.”14

Naturally we address the YFs such as the belief hurt = harm and that activity is harmful. This is key to reconceptualizing pain and danger versus safety signals. Deimplementing scare tactics about their imaging pathology and giving them a positive experience with movement builds their self-efficacy so they are less PROTECTIVE.

Establish trust to build movement confidence by identifying painful activities and then training around pain using our principles.

  • Principle 1: Reassurance: Not every hurt = harm. Traffic light. >5/10 red light.

  • Principle 2: Reactivation: Move well then move often but don’t try to teach perfect patterns; functional movement screen (FMS) 2 (acceptable compensation) is good. Avoid 0s (red light pain) or 1s (unacceptable form). 3 (perfect form) is unnecessary if not loading.

  • Principle 3: Resilience: Add load to cause adaptation. Rating of perceived exertion at least a 5/10—rated as “hard” or where breath begins to change from low to higher threshold strategy.

  • Principle 4: Variability: Vary both the task and the environment. Let person be like child and explore movement—play. Give varied options including unexpected things. Be creative. Should include activities mirroring the hardest passages of play or life activities that could potentially occur.

Integrating the Four Principles into the Clinical Process

Three steps

  • History

  • Examination

  • Education/Treatment/Training


  • Chief complaint

  • Onset

  • Mechanism of injury

  • Imaging

  • Treatment (past and current)

  • Past history

  • Related medical history

  • Activity intolerances (measure—patient-specific functional and pain scale; see Chapter 8 Appendix)

  • Progress (measure with responsive tools)

  • Occupation

  • Past and current physical activities

  • How does their condition affect them?

  • What do they think is wrong?

  • What do they think will help?

  • Expectations

  • Beliefs/fears (protection) (measure with yellow flags—see Chapter 7 Appendix 7A)

  • Goals (why behind the what)

  • Current activity load (measure weekly rating of perceived exertion [RPE], frequency, and duration) (see Fig. 37.29A and B)

  • Repeat back to patient what they’ve said for confirmation that you heard them correctly

  • Always ask if there is anything else that they believe may be important.

  • Patients are asked to rate their willingness to change: lifestyle, exercise, diet, etc.

Patients rate their perceived stress and quality of sleep (measure: Wellness Questionnaire).15,16,17 (See Appendix Form 5).

  • Medications and supplements

Goal: Build trust and relatedness


  • Education (reassurance—MRI, hurt and harm, protection, safety, preparation). Principle 1—reduce fragility, traffic light analogy (see chapter 38).

  • Stress, sleep, mental/emotional state all have an effect on pain. They can all be targeted to help reduce pain—“there’s more than one road to Rome.”

  • Inactivity leads to more arthritis.

  • Activity slows the aging process: It’s not “wear & tear”!

  • Good stress is needed to create adaptation: “No strain no gain.”

  • Overprotection LEADS to underpreparation!

  • Explain “gift of injury”—the silver lining is that they will recover and this will help them develop resilient, sustainable approach for the future.

  • Explain that one’s “biography becomes their biology”… but it is reversible.

  • Lifestyle can lower biologic age over 15 years.

  • Increase quality of life so that health span lasts a lifetime.

  • Principle 2—reduce overprotection. Calm things down—graded exposures—“every exercise is a test.”

  • Supplementary treatments may be appropriate in the case of acute symptoms or as a catalyst in recurrent or chronic situations (manual therapy, traction, passive modalities, medication, interventions, etc.).

  • Sparing strategies—hygiene. Be sure to relate to patient’s specific individualized activities of daily living (ADLs), work-related duties, sport-specific tasks.

  • Principle 3—building resilience—Hardest thing you do well to improve the weakest link nested to the chief complaint. Sufficient intensity is necessary to cause adaptation.

  • Principle 4—Variability—Options, exploration, and play. DST, gamification, and regional interdependence. Improving movement literacy, prepare for the unexpected.

Goal: Build confidence and give hope

The Disability Problem

Lower back and neck pain were the leading global cause of disability in 2015 in most countries.18 This was verified by the Global Burden of Disease Study covering 1990 to 2017 data.19 Noncommunicable diseases (NCDs) accounted for 18 of the leading 20 causes of age-standardized YLD on a global scale. Aging of the world’s population is increasing the number of people living with sequelae of diseases and injuries.

“About 5% of those under the age of 18 years have some activity limitation, 40% by age 65, and 55% 85 and over.”20

The burden of disease methodology was developed by researchers at Harvard and the WHO to quantify the amount of premature mortality and disability present in a population. Disability-adjusted life years includes the number of years lost to ill health, disability (YLD) or years of life lost to premature death (see Fig. 39.12).

Figure 39.12 Global burden of disease in 2017. From Global Burden of Disease Collaborative Network. Global Burden of Disease Study 2017 (GBD 2017) Incidence, Prevalence, and Years Lived with Disability 1990-2017. Seattle, WA: Institue for Health Metrics Evaluation. Used with permission. All rights reserved.

Although substantial progress has been made toward reducing mortality and extending life expectancy throughout the world over the past few decades, the epidemiologic transition is manifest in the growing importance of nonfatal diseases, outcomes, and injuries, which pose, partly as a consequence of decreasing death rates, a rising challenge to the ability of the world’s population to live in full health.

For the first time in human history, in 2020, there will be more older persons alive than children (see Fig. 39.13).21

In middle-aged adults, musculoskeletal disorders dominated the top rankings followed by mental health disorders, especially depression. Diabetes and sense organ disorders were found to be prominent causes of disability in middle age. In older adults (older than 65 years), sense organ disorders were the top-ranked cause of disability. Musculoskeletal disorders remained a dominant source of disability, and chronic obstructive pulmonary disease entered the top ten. In the oldest age groups, ischemic heart disease and Alzheimer’s and other dementias made their first appearance in the top ten.

According to the recent Lancet Commission report, “These three pandemics—obesity, under-nutrition, and climate change—represent The Global Syndemic that affects most people in every country and region worldwide.”22 They go on, “They constitute a syndemic, or synergy of epidemics, because they co-occur in time and place, interact with each other to produce complex sequelae, and share common underlying societal drivers.” Musculoskeletal pain-related disability and the worldwide sedentarism are similarly part of a syndemic.

Figure 39.13 Population demographics. Y-axis represents percentage of the population at a given age. X-axis represents the year.

Inactivity: Underpreparation

Recently, studying masters athletes has given us insight into the nature of aging and its physical effects. Many assume that physical activity can reverse or slow down the aging process, and we confuse the effects of inactivity with the aging process itself, believing certain diseases are purely the result of getting older. In reality, it is not the 80-year-old athlete who has the physiology of the 50-year-old inactive person that is slowing the aging process. They are exactly as they should be. It is the 50-year-old inactive person that is speeding things along.

Steve Harridge, coauthor and professor of physiology at King’s College London, said: “Being sedentary goes against evolution because humans are designed to be physically active.”23 Evolutionarily speaking, our bodies are designed to be active throughout the entire lifespan. Our modern sedentary lifestyles have essentially sped up age-related decline and contributes to onset of disease such as type 2 diabetes, cardiovascular disease, and cancer. Allowing progression of this plight is that we have been able to rely on “the crutch” of modern medicine to get away with problems related to inactivity.

Endurance cyclists in their 80s have the immune systems of people in their 20s.14 The elderly endurance cyclists

  • Produced the same level of T cells as adults in their 20s

  • Compared to a group of inactive older adults were producing very few T cells

Duggal et al24 reported that “Aging is accompanied by a decline in immune competence, termed immunesenescence, which is characterized by an increased risk of infections and chronic inflammatory
diseases…. The mechanisms underlying this compromised immunity include involution of the thymus, which begins in early adulthood in humans and accelerates rapidly after 40 years of age.”

The Immune System and Aging

“The immune system declines by about 2-3% a year from our 20s, which is why older people are more susceptible to infections, conditions like rheumatoid arthritis and, potentially, cancer.”25

Professor Janet Lord, director of the Institute of Inflammation and Ageing, the University of Birmingham

Regular physical activity in older adults has been associated with14

  • lower levels of proinflammatory cytokines such as interleukin-6, tumor necrosis factor α;

  • improved neutrophil chemotaxis and natural killer cell cytotoxicity;

  • increased T-cell proliferation;

  • higher frequency of naive T cells;

  • improved vaccination responses.

Physical activity is shown to be thymoprotective and preventive of thymic involution, thus helping the immune system adapt to novel pathogens in the environment.14 Duggal’s group14 report that “aging is a complex process involving the interaction of a number of factors, including genetics, environment and lifestyle. Our findings highlight that physical inactivity with age may be a profound driver of several aspects of immunesenescence, most notably reduced thymic output, changes to regulatory cell frequency and function and T-cell polarization.” Reduction in thymic output has been suggested as a determinant of mortality in older adults.26

From age group to age group, the average person is not meeting physical activity recommendations: “In England fewer than half of 16-24 year olds meet the recommendation for aerobic and muscle strengthening exercises; for 65-74 year-olds, it falls to fewer than one in 10.” Although this is nothing new, research is not only suggesting that active younger people keep their activity levels up through the aging process, but that 40-year-olds who begin to increase their physical activity levels can also reap similar benefits.27 Physical inactivity is a pandemic affecting people all over the world.28 The Lancet study on Worldwide trends in inactivity reported that, “Insufficient physical activity is a leading risk factor for non-communicable diseases, and has a negative effect on mental health and quality of life.”28 Some key points from the report:

  • The 2025 global physical activity target (a 10% relative reduction in insufficient physical activity) is at risk.

  • Policies to increase population levels of physical activity need to be prioritized and scaled up urgently.

  • Data representing 96% of the world’s population show that globally more than a quarter of all adults in 2016 were not getting enough physical activity.

  • In wealthier countries, sedentary occupations and individual transportation vehicles are the major culprit.

  • The largest increases in insufficient physical activity have occurred in high-income countries.

  • The main improvements are due to increased participation in physical activity in China.29 most likely due to increased park use and physical activity among China’s rapidly growing elderly population.30

Global Action Needed to Address the Global Inactivity Crisis

“A significant increase in national action is urgently needed in most countries to scale-up implementation of effective policies. The Global Action Plan on Physical Activity 2018-2030,30 is a new catalyst for global action, and provides a selection of 20 specific policies targeting different settings and populations that can be adapted and tailored to local contexts in all countries. However, implementation will require bold leadership and full engagement across sectors to change the current approach.”28

Further research suggests that “maintained physical activity into middle and old age protects against many aspects of immune aging which are in large part lifestyle driven.”24 Along with benefits for the individual, being more physically active has societal benefits as well. “The number of people aged 65 and over is projected to rise by more than 40% in the next 16 years. The average 85-year-old costs the NHS more than five times as much as a 30-year-old, analysis suggests.”32

These data are becoming more and more pertinent because globally, the population is living longer lives, but not necessarily maintaining quality of health in their later years. “The number of people aged 65 and over is projected to rise by more than 40% in the next 16 years.”33 “Many benefiting from projected life expectancy increases by 2035 will spend their extra years with four diseases or more, according to a study in England.”

Exercise is the only “medicine” we have to combat some of the biggest factors in loss of physical function because of aging: loss of muscle mass, loss of strength, declining balance, and along with it increased risk for falls. Studies also suggest that resistance training (RT) can benefit

  • bone mineral density34,35

  • lipoprotein profiles36

  • glycemic control37

  • body composition38

  • symptoms of frailty39

  • metabolic syndrome risk factors40

  • cardiovascular disease markers41

Furthermore, RT not only has physiologic benefits, but also benefits of psychosocial health:

  • sense of coherence42

  • perceived stress43

  • depression44

  • anxiety45

  • fatigue46

Behavioral Nudges Are Key

“No longer is it acceptable for a physician to tell a patient to get more exercise…. We need to focus on lifestyle and behavior modification to overcome some sedentary behaviors. We cannot and should not be telling our chronically inactive friends, neighbors, clients, patients or students to simply go to a gym or get more exercise. For some that will work, but for most it will not. An alternative is to make small changes in behavior and small changes in lifestyle to increase physical activity. Taking the stairs instead of the elevator when going up or down one or two flights or parking the car in the last row instead of the first one at the grocery store are just a couple of examples.”

Walter R. Thompson, PhD, FACSM, currently serves as the immediate past president of the American College of Sports Medicine

Overprotection, Nocebos, and Reassurance

Overprotective advice leads to rigidity (i.e., “safety behaviors” and avoidance), whereas coping is equated with a “flexible” mindset. In this context variability of DST is a fundamental principle for positive coping.47

The precision person-centered approach is based on looking at the individual and their environment.48,49 Psychological and social factors as well as pathology and symptoms are all important. The modern BPS approach is guided by nudging behavior toward higher volumes (Principle 2), intensity (Principle 3), and variability (Principle 4) of activity in order to change beliefs about the relationship of activity and pain or hurt and harm (Principle 1). Changing beliefs (i.e., cognitions) is in a yin-and-yang relationship with changing activity tolerance.

The dichotomy between a biomedical and BPS paradigm is artificial, and as some have suggested, the BPS model still suffers from phenomenologic issues.49 The downside of the biomedical approach is that “it inaccurately endorses a linear relationship between noxious stimuli and pain, and is often dualist or reductionist…. From a reductionist perspective, pain is often considered to be ‘in the brain.’”49 Similarly, the BPS model is weakened by the fact that the “boundaries between the biological, psychological, and social are artificial, and the model is often applied in a fragmented manner. The model has a limited theoretical foundation, resulting in the perpetuation of dualistic and reductionist beliefs”49 (see Fig. 39.14).

Pincus et al reported that the BPS model has been misunderstood and therefore poorly applied. According to Low, “This may be because the bio-psychosocial model fails to explain the body/mind problem, with the biomedical paradigm on one side and the psychological and social perspective on the other with no clear theoretical link between them.”50 As described in Chapters 1, 5, and 38, clinicians have compartmentalized patient presentations into bio, psycho, or social rather than taking a person-centered approach as described by Vaz et al.48 The greatest oversight is the failure to include the person’s environment as the key milieu within which context gives value to experience of potentially disabling pain.48

Figure 39.14 Reductionist and dualist nature of the biopsychosocial model and the proposed environment-person model solution.

Worst of all, if imaging is negative or treatments aimed at hypothesized pathologic structures fail to give relief, the HCP mistakenly blames failure to get better on the patient! This is tragic precisely because our ability to be certain that we have accounted for the vast complexity of interacting variables gives us an insurmountable cognitive or confirmation bias.

According to Stilwell and Harman,49 an enactivist interpretation appreciates the first-person experience of pain and disability and thus avoids the mereologic fallacies of either

  • a dualistic approach (structural pathology—bio or psychological illness behavior—psycho) or

  • the trichotomization of pain resulting from the BPS approach

The enactive approach distinguishes itself from both the biomedical and BPS approaches to pain because49

  • “(it) has a strong theoretical foundation with important elements not found in other pain theories such as recently converging theories of perception (i.e., embodied cognition and predictive processing)”

  • “These elements of the enactive approach are interconnected and dependent on each other, in contrast to the biopsychosocial approach that does not have this explicit interconnectivity.”

Stilwell and Harman49 summarize the enactive approach in a thought-provoking relational manner: “… pain does not reside in a mysterious immaterial mind, nor is it an entity to be found in the blood, brain, or other bodily tissues. Instead, pain is a relational and emergent process of sense-making through a lived body that is inseparable from the world that we shape and that shapes us.” This hypothesis leaves much unanswered; however, it should help us to realize that the BPS construct is not a panacea to limitations inherent in a biomedical approach.

Taking a practical approach, what can we measure? Examples of actionable and relatable goals include activity levels, beliefs about the relationship of activity and pain, hurt and harm, and sensitivity versus tolerance. Inactivity is the upstream issue leading to
underpreparation and is intertwined with overprotection. Inactivity is on the rise and related to our modern disability crisis.

We are fighting vested interests, overdiagnosis, the opiate crisis, myths about the inevitability of “wear and tear,” and various other hypes, trends, and urban myths in physiotherapy, rehab, and chiropractic.3,4,5,54 New weapons such as PMCS and the cognitive-functional training approach are part of a pain revolution, giving people hope, self-efficacy, and a positive experience with movement.55,56 The challenge is transfer of knowledge from the scientific realm to the practitioner.57

The Future of Integrating Complex Systems Theory into Practice

LBP is multifactorial, having biologic, psychological, and social components. Yet, seeing these as operating independently is an artificial construct.49,50,52 Putting this into practice is a challenge.58

According to Cholewicki et al,59 “To study very complex problems and the effects of specific solutions under various conditions, a ‘system’ approach is advocated whereby the entire system’s behavior is being studied, including the interactions among its elements (in contrast to a reductionist approach whereby a system is broken down into smaller elements, which are then studied in isolation).60 Dynamic systems theory has been used to study the impact of various policy interventions to reduce opiate medicine drug abuse for pain management.”61

A major obstacle in implementing a systems approach to the BPS management of LBP is that knowledge tends to congregate in the individual domains—biomedical or biomechanical, psychological, or social—rather than be integrated.59 Attempts to integrate knowledge across several domains of LBP have mostly been limited to qualitative and descriptive models.62,63,64 Cholewicki et al59 “describe the process of identifying and refining the composition and structure of such a model, which constitute the first step in the systems approach…generating individual models (‘mental models’65) of participants with diverse expertise in LBP using fuzzy cognitive mapping (FCM)….”66,67

The Kinetic Chain and Regional Interdependence

Functional training should focus on the source of biomechanical overload rather than just where weakness or tightness exists. Too often athletes receive an endless array of exercises to “fix” a problem. For instance, a knee issue will be addressed with various stretching or strengthening exercises but the injury does not respond because the problem was coming from another link in the kinetic chain! If subtalar hyperpronation is the cause of medial collapse of the knee and valgus overload, then no local approach to the knee itself is going to help. Therefore, a functional evaluation should identify the source of biomechanical overload in the kinetic chain before a training plan commences so that the “key link” can be unmasked.

Loss of force transfer at any link of the kinetic chain may lead to “energy leaks,” decreased performance, and resulting injury. Normalizing specific dysfunctions of any movement pattern including the associated joint, muscle, or fascia will likely facilitate improved performance. Mobility deficits of the thoracic spine and hip, and stability deficits of the lateral hip/pelvis and core deserve to be highlighted for their influence throughout the locomotor system.

Identification of painful markers, MSs, painless dysfunctions, signs of abnormal motor control (AMC), and evaluation of training load are important aspects of the assessment process but must be considered within a broader BPS framework. Dr. Lewit acknowledged this in stating “…psychological factors play a great role, as motor patterns are to a certain degree expressions of the state of mind: anxiety, depression and an inability to relax… no less important is the subject’s psychological attitude to pain.”68

The “key link” in the patient encounter often extends beyond the kinetic chain to include the patient’s beliefs and mindset. In many cases, the rehabilitation of a painful spine condition may have more to do with reconceptualizing the person’s beliefs about their spine rather than changing tissues related to the spine. Therefore, the art of training involves not only the quality of movement produced by the locomotor system and the load that system is exposed to but also the thoughts, beliefs, and motivations of the human undergoing the training.

An interesting study by Littlewood and Cools69 offers a skeptical perspective on the relationship of AMC and painful conditions. “The review reports that 65% (104/160) of those with scapular dyskinesis did not go on to develop shoulder pain, whereas 25% (65/259) of those without scapular dyskinesis did.”

A meta-analysis review reported that scapula-focused approaches for shoulder pain “confers benefit over generalized approaches up to six weeks but this benefit is not apparent by 3 months. Early changes in pain are not clinically significant. With regards to scapula position/movement, the evidence is conflicting.”70

A comparison of three factors on shoulder injury rate in elite youth handball players was undertaken71 (see Fig. 39.15):

  • A sudden large increase in load defined as >60% relative to the weekly average amount of handball load the preceding 4 weeks

  • Reduced external rotational strength

  • Scapular dyskinesis

An increase in handball load by >60% was associated with greater shoulder injury rate (hazard ratio [HR] 1.91; 95% confidence interval [CI] 1.00 to 3.70, P=0.05) compared with the reference group. The effect of an increase in handball load between 20% and 60% was exacerbated among players with reduced external rotational strength (HR 4.0; 95% CI 1.1 to 15.2, P=0.04) or scapular dyskinesis (HR 4.8; 95% CI 1.3 to 18.3, P=0.02). Reduced external rotational strength exacerbated the effect of an increase above 60% (HR 4.2; 95% CI 1.4 to 12.8, P=0.01). If load increased by less than 20%, there was no increased rate of injury even in those players with scapular dyskinesis or reduced ER strength. They concluded, “A large increase in weekly handball load increases the shoulder injury rate in elite youth handball players; particularly, in the presence of reduced external rotational strength or scapular dyskinesis.”71

McQuade et al72 summarize the prevailing theory regarding scapular stabilization:

  • the scapula must provide a stable base upon which upper extremity tasks are accomplished;

  • without scapular stability there is increased risk for pathologies such as impingement or cuff tears;

  • dyskinesia is a sign of instability and is a result of weak or unbalanced scapulothoracic (ST) muscles.

McQuade et al72 dispute the above idea and state a modern reconceptualization, “it may be more accurate to conceptualize ST function as an energy transfer system rather than an anatomical structural base of support.” The authors continue, “There are several arguments against considering dyskinesia to be an indicator of instability. First, we propose that most observed scapular dyskinesia likely represents normal movement variability.”

Figure 39.15 Weekly load increases. Adapted from Møller M, Nielsen RO, Attermann J, et al. Handball load and shoulder injury rate: a 31-week cohort study of 679 elite youth handball players. Br J Sports Med. 2017;51:231-237.

The authors conclude, “the current clinical scapular stabilization paradigm is ambiguous, is flawed, and has limited support from current evidence. The notion that there is an ideal scapula orientation or that isolated ST muscle strengthening will be effective for people with dyskinesia is also unsupported.”

Head/Neck Posture Influences

On neck pain The combination of manual therapy and stabilizing exercises was more effective than stabilizing exercises alone.73 Both approaches were superior to a general exercise program. Improvements were noted in both pain reduction and forward head posture (FHP) and round shoulder posture, evidence of an important link between the neck and shoulder in function of the kinetic chain. One-month follow-up showed the results were maintained.

Richards et al74 found no link between cervical spine posture and neck pain or headaches in a study of over 1,100 adolescents. The study included commonly hypothesized postural faults such as forward head and slumped postures.

Thoracic Spine Influences

On the shoulder Thoracic spinal manipulation has been shown to be helpful for patients with shoulder impingement syndrome.75,76,77 In one controlled study, it was shown effective by itself.78 There is evidence of the relationship between the thoracic spine and the shoulder kinematics.

On the neck It has been demonstrated that a significant association exists between decreased mobility of the thoracic spine and the presence of patient-reported complaints associated with neck pain.79 Cleland et al80,81 showed that in selected patients, manipulation of the thoracic spine was a successful treatment for patients with neck pain.

Lumbopelvic Influences

On the upper quarter There was a greater reduction in upper trapezius activity after pelvic tilt reduction during arm elevation, thus suggesting a connection between the lumbopelvic region and shoulder/neck regions.82

Hip Influences

On the lower back Lateral hip instability and posterior hip mobility deficits are functional problems that influence areas above and below it. For example, the hip abduction test can predict individuals who are at risk for LBP development during prolonged standing.83

  • Whitman et al84 found that treatment of the hip was successful in the management of spinal stenosis.

  • Cibulka et al85 reported that unilateral deficits in hip range of motion were associated with sacroiliac pain syndromes.

  • Frost86 reported that exercise band training designed to facilitate greater gluteal activation did so while sparing the spine.

A large study of professional baseball players demonstrates association between hip mobility and injury risk of the core and low back. “A total of 258 player-seasons (129 pitchers and 129 position players) resulted in 20 back and 35 abdominal injuries across all players and 28 elbow and 25 shoulder injuries in pitchers. Hip ROM did not correlate with shoulder or elbow injuries. Hip internal rotation deficit of 5° correlated with core injury (odds ratio [OR], 1.40; P = 0.024 for pitchers; OR, 1.35; P = 0.026 for position players) and back injury (OR, 1.160; P = 0.022 for pitchers).”87

On the knee Cliborne et al88 found that hip dysfunction was correlated with knee pain associated with arthritis and that hip mobilization was beneficial in these patients. Improvements in hip flexion strength, combined with increased iliotibial band and iliopsoas flexibility, were associated with excellent results in patients with patellofemoral pain syndrome.89

In a recent meta-analysis, the link between hip strength and dynamic knee valgus is conflicting based on what task (single leg squat, single or double leg ballistic) is assessed.90 However, in single leg ballistic demands, the relationship is more robust.90

Knee valgus is challenging to measure reliably. When using the Microsoft Kinect 2.0 skeletal tracker (a widely used tool for inexpensive, portable measurement function) for measuring osteokinematic joint angles of the hip and knee, a number of limitations
have been demonstrated.91 According to the authors, “Non-sagittal hip and knee angles did not correlate well for the drop vertical jump.” For other measurements, it did show that it can provide limited three-dimensional kinematic information of the lower limbs that may be useful for some functional movement assessments.91

According to Paterno et al,92 “participants who sustained a second ACL injury had increased 2-dimensional peak frontal plane knee motion during the landing phase of the drop vertical jump (DVJ).” Performed from a 31-cm box with three trials (see Fig. 39.16A and B), this test has been shown to be highly reliable.93

Rabelo and Lucareli94 reported that

  • Hip muscle weakness may be a consequence of and not the cause of knee pain

  • Kinematics posttreatment are not related to pain or disability

  • Hip muscle weakness does not appear to be causally related to dynamic knee valgus

  • Mechanical factors are likely to be overestimated

  • A BPS approach is recommended

Figure 39.16A Drop vertical jump in males and females: representative of valgus at landing in female compared with male athlete when performing landing tasks. Reproduced from Hewett T, Myer GD. In: Liebenson C, ed. Prevention of Knee Injury in Women from Functional Training Handbook. Wolters Kluwer; 2014.

When investigating capacity tests and performance—in youth female soccer players—it has been shown that the single leg countermovement jump (SLCMJ) appears to be the most sensitive jump test for identifying asymmetries that correlated with 5-, 10-, and 20-m sprint times.95 The presence of a minimum of 12% asymmetry side to side was sufficient to showing negative associations. It was compared to a series of horizontal jumps for distance—single, triple, and crossover hops. Scoring the test using the “My Jump” iPhone application has been shown to be reliable.96

The first point to consider from these results is that the SLCMJ produced significantly greater asymmetries than all other jump tests, which is in agreement with previous research which showed that vertical jumping showed greater asymmetry than horizontal jumping.97

Unilateral jump tests are easy to administer and ecologically valid, especially for team sport athletes. The SLCMJ appeared to be the most appropriate test for identifying interlimb asymmetries in youth female soccer players, and these differences are associated with slower sprint times.

Figure 39.16B Drop vertical jump maneuver—side view. Reproduced from Hewett T, Myer GD. In: Liebenson C, ed. Prevention of Knee Injury in Women from Functional Training Handbook. Wolters Kluwer; 2014.

Core Influences

On the knee Athletes with decreased neuromuscular control of the body’s core, measured during sudden force release tasks and trunk repositioning, are at increased risk for knee injury.98,99 Specifically, impaired trunk proprioception and deficits in trunk control have been shown to be predictors of knee injury.98,99

On the hamstrings A rehabilitation program consisting of progressive agility and trunk stabilization exercises was found to be more effective than a program emphasizing isolated hamstring stretching and strengthening, in promoting return to sports and preventing injury recurrence in athletes suffering an acute hamstring strain.100

On LBP A brief review of the literature highlights some problems with the assumption that core stability training is superior to other active approaches for managing LBP. Exercise has been shown to be effective for LBP.3,4,5,54,101 Strength training has been shown to be beneficial but only for full body programs.102 Increases in activity have been shown to improve LBP and form the standard of care.103,104 According to Augeard and Carroll,105 “the claim that core stability exercise is one of the most effective options for low-back pain is without merit and clearly lacks supporting evidence.” Core stability changes do not predict improvements in disability following specific exercise.106

In conclusion, regional interdependence has great plausibility, yet the evidence is controversial. The danger of confirmation bias is seeing motor control training or the joint-by-joint approach as essential when in fact it is merely an option. The downside of such certainly is “rehab purgatory” (see Chapter 38) where we fail to progress from Principle 2 to Principles 3 and 4. Regional interdependence if used to promote a ramp to building robustness make sense as a viable option (see section on Accessory Menus). For instance, the role of thoracic, hip, or great toe mobility is shown as a springboard for building capacity. Similarly, isometric torso training during overhead tasks or single leg landing may be a decisive component of successful rehabilitation.

Patient Education

Against best practices for the treatment of LBP, typical management today includes excessive imaging and excessive FOCUS ON symptom relief. In both cases, a missed opportunity occurs to educate patients about the positive natural history of LBP and resilience of the human body.

O’Keefe and O’Sullivan say, “the medicines we call ‘painkillers’ are not very effective at treating low back pain and often come with significant side-effects.”

“The problem isn’t getting the scan, but rather what people are told about it and what happens next.”107

Although the standard of care is slowly improving because of new research regarding the efficacy of mainstream treatment methods, there is still a lot of room for improvement. For clinicians, understanding the mechanism of pain as well as the factors that affect pain is beginning to alter the way LBP is managed. The prognostic significance of psychosocial factors is becoming better understood, yet clinicians are still not addressing these factors directly when managing these cases.

This can be done by

  • Explaining that imaging is not required and will not change management

  • Avoiding using terms such as injury, degeneration, or wear and tear

  • Encouraging the patient to stay active and avoid bed rest, continue daily activities, stay at work or return as soon as possible

  • Encouraging the patients to take responsibility for their own continued management by developing positive coping strategies and self-managing their symptoms

  • Avoiding language that promotes fear of pain and catastrophic thinking (e.g., “let pain be your guide,” “stop if you feel pain,” and “you have to be careful”).

Change has to be a grassroots effort to create a societal shift on LBP management, not just by educating clinicians but by reinforcing those recommendations by changing reimbursement strategies, vested interests, and the financial and professional status quo. Huber and colleagues propose adoption of “Positive Health” as a strategic approach to prevention of long-term disability from LBP. Positive health, Huber says, is “the ability to adapt and to self-manage, in the face of social, physical, and emotional challenges.”

Societally, initiatives are needed to change widespread and inaccurate beliefs about back pain, such as counterproductive patterns of illness behavior, for
example, prolonged rest, avoidance of usual activities, or staying away from work.

In the occupational setting, there needs to be peer support for the notion that LBP is not an injury in need of medical treatment108 and that the public and patients should adjust expectations so that people are less likely to anticipate a diagnosis or a complete cure for their pain.

Improved training and support of primary care doctors and other professionals engaged in activity and lifestyle facilitation, such as physiotherapists, chiropractors, nurses, and community workers, could minimize the use of unnecessary medical care.

Along with this, system changes integrate and support the health professionals from diverse disciplines and care settings to provide patients with consistent messages about mechanisms, causes, prognosis, and natural history of LBP. Including active strategies such as exercise are associated with reduced disability and less reliance on formal health care.

According to Maher (in Mackee109), “The contemporary approach relies on a smaller set of red flags than previously and emphasizes the use of clusters of red flags along with clinical expertise to guide decision making.”

It’s important to identify people who have YFs and are at high risk of having persisting problems, as well as people who just need advice to keep moving and how to manage pain themselves. There are several free risk evaluation tools accessible to clinicians to help with this process. These tools include:

  • Keele STarT Back Screening Tool110

  • Örebro Musculoskeletal Pain Screening Questionnaire111

  • PICKUP calculator112

O’Keefe and O’Sullivan say, “Overall, people should try to use their back sensibly and build up tolerance to certain activities like bending and lifting through practice with different loads and weights. But people shouldn’t wrap their back in cotton wool and avoid activities. The back, like all body parts, is designed for movement and will adapt to different activities and loads with practice.”109

What Is the Primary Function of Hominoids?

The question of hominoid or Homo sapiens function is important because in our modern world we have diminished our activity levels so dramatically. Although speech, prehension, and other functions are clearly unique, one can argue that what is most unique from a physical perspective is that humans are upright and volitionally move in a primarily unipedal fashion. Running, for instance, is a great strength of hominoids and has served our evolution well by enabling us to find alternate food sources as foragers and later to hunt.

The subject of evolutionary biology is vast, complex, and far beyond the scope of this section. However, a deep understanding of human health/disease, function/dysfunction is contingent upon knowledge of why and how humans evolved in the first place.

The first life sprung forth on earth approximately 3 billion years ago (see Fig. 39.17) and has advanced from aquatic to amphibious (600 million)
to reptilian (250 million) to mammalian (75 million) to human. If imagined as a 24 hour clock human life has only emerged in just over the last minute of the day! Dinosaurs just before 11:00 PM; land plants just before 10:00 PM; single celled algae around 2:00 PM; the oldest fossils around 5:30 AM; the origin of life at 4:00 AM.

Figure 39.17 History of life timeline.

This list shows the progression from fish to hominoid:

  • Aquatic animals have vestigial scapulae (fins). Fish are uniplanar, whereas amphibians and reptiles became biplanar.

  • Quadruped mammals ground reaction force (GRF) vector moves through their mid-torso, apes when walking in front of their hips and behind their head, whereas hominoids GRF vector travels from the foot all the way cephalad through their hip, sternum and head.

  • Birds and mammals are triplanar.

  • Bipedalism and climbing evolved with the apes. The frontal plane dominates in locomotion.

  • Unipedal walking and running appeared with hominoids. According to Austin Einhorn, “our heel is meant to be on the ground, excessive plantar-flexion is a compensation.”113

It is believed that the family Hominidae, including humans and great apes, began their evolution 8.5 million years ago, whereas human and chimp divergence – or the “last common ancestor” between hominoid and ape – occurred between 8 and 5 million years ago.114 Hominins are defined as all species more closely related to living humans than to chimpanzees or other apes.114 The genus Homo includes modern and archaic humans, with the species sapiens containing only modern humans. The modern human or Homo sapiens appeared approximately 200,000 to 250,000 years ago on the evolutionary timeline (see Fig. 39.18).

Figure 39.18 Ape-human bifurcation.

Why a Larger Brain?

It has been theorized that the emergence of modern primates with larger brain sizes has been because of visually guided reaching, grasping, and other forelimb action. Isbell115 postulated that the decisive evolutionary adaptation leading to a larger brain was the emergence of the ability to detect predators—such as snakes—preconsciously and thus to act on those perceptions. This led to the expansion of the visual system and visual cortex and, consequently, increased brain size. Over one-half of the neocortex is associated with vision, thus leading to the much larger brain size of humans.116 According to Huynh Sanh Thong, a MacArthur fellow, snakes were responsible for the origin of language because mothers had to warn their children about them (Thong117 in Isbell115).

Declarative Pointing, Language, and Hominoid Evolution

“Snakes gave bipedal hominins, who were already equipped with a non-human primate communication system, the evolutionary nudge to begin pointing to communicate for social good, a critical step toward the evolution of language, and all that followed to make us who we are today.”115

According to Isbell,115 neither gesturing in chimps nor bipedalism in hominoids led to language; “it is not clear how bipedalism per se would have operated as a selective pressure favoring language.” It is a social activity and precursor of language.115 Declarative pointing is unique to hominoids whereas chimpanzees utilize gazing, general gesturing, and grunting for social communication.115

  • Declarative pointing is a developmental precursor to language.

  • Babies point before they speak.

  • Babies who gaze longer and point where their mothers gaze acquire language at a faster rate by age 2.118

  • An 8-month-old baby’s response to their mother’s gaze and pointing predicts vocabulary development at 30 months.119

The key link from declarative pointing toward having a larger brain is mediated through what we see (and thus the visual cortex). Having increased cortical fear centers in order to assist in predator avoidance also contributed to the expansion of the visual cortex and the development of larger brains in modern primates. “For any given body weight, primates have twice as much brain tissue as most other mammals” (Martin120 in Isbell115). Brain tissue is highly metabolically active. Change in brain size has been shown to correlate with the highly metabolic visual pathway neurons such as cytochrome oxidase (CO). CO is “an enzyme complex in the mitochondria that deals with electron transport and is critical for aerobic energy metabolism” (Kadenback121 in Isbell115).

Isbell suggests that increased dietary glucose (fruits and nectar) helped to develop and enhance our visual processing pathways. Glutamate is the main excitatory neurotransmitter in the central nervous system; however, it can be toxic.123 If there is not enough glucose or CO, glutamate is released presynaptically causing a malfunction in energy metabolism.124 Isbell states, “the glucose in fruits protects the K and P pathways from glutamate excitotoxicity.”

Being able to see ripe fruits freed hominoids from dependence on olfaction to find foods and “permitted the metabolic and neurological expansion of primate visual systems.”115 Visual acuity, depth perception, and the ability to discern patterns and shades were not only needed to identify ripe fruits, but also a necessity to stay ahead in the predatorprey arms race by being able to avoid new camouflaged venomous snakes. Primates utilize the visual K pathway for fast preconscious detection of predators. It allows primates to read situations and react in an agile manner based on a threat assessment of visual cues such as if a social engagement is friendly or antagonistic. Isbell argues that “our excellent vision is mainly the result of evolutionary pressure to detect and avoid snakes.”115

Why Bipedalism?

Through this divergence of humans and apes, numerous distinguishing structural and functional characteristics are evidenced but few are more relevant than bipedalism, when an organism moves by means of its two rear limbs such as human legs/feet. Although apes and other animals do occasionally stand and walk on two feet, habitual bipedalism, as seen in humans, is rare. Darwin125 believed that bipedalism was the spark that set the human lineage off on a separate evolutionary path from the other apes.

“Man could not have attained his present dominant position in the world without the use of his hands, which are so admirably adapted to act in obedience to his will.… But the hands and arms could hardly have become perfect enough to have manufactured weapons, or to have hurled stones and spears with a true aim, as long as they were habitually used for locomotion and for supporting the whole weight of the body, or, as before remarked, so long as they were especially fitted for climbing trees….”125

Darwin’s125 reasoning for why this form of locomotion was selected (freeing up the hands) has been questioned but it is undeniable that bipedalism set hominids on a very different evolutionary path.

Evolutionary biologist Daniel Lieberman reminds us in The Story of the Human Body that “just as the tough get going when the going gets tough,
natural selection acts most strongly not during times of plenty, but during times of stress and scarcity.”114 It is impossible to know exactly why natural selection favored adaptations for bipedalism, but the majority of evidence points toward a change in climate as the driving force behind the selection of regular upright walking. This adaptation would serve to assist hominids in obtaining food more readily. Between 10 and 5 million years ago, the entire earth’s climate cooled considerably and the overall effect in Africa was to cause rainforests to shrink and woodland habitats to expand.126 Those living on the edge of the rainforest would have had to travel farther to obtain adequate food and nutrition.

“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.” — (Charles Darwin)

There are several other popular theories as to why bipedalism was favored in the first hominids, such as to see over tall grass, swim, and improved abilities to make/use tools, but few of these hold up under scrutiny.114

Advantages of Bipedalism?

Two advantages of bipedalism are an improved ability to forage and an improved locomotion efficiency. An erect posture would have allowed hominids to reach for hanging fruits by straightening their knees and holding on to a branch.127 In this way, standing upright on two feet may have initiated as a postural adaptation. The second advantage of bipedalism is energy conservation. Knuckle walking on all fours is energetically an expensive way to get around. Lab studies have demonstrated that chimps walking on treadmills spend four times more energy compared to humans to cover a given distance.128 Lieberman114 states this difference occurs because chimps have short legs, they sway from side to side, and they always walk with bent hips and knees. As a result, chimps constantly spend lots of energy contracting their back, hip, and thigh muscles to keep from toppling over and collapsing to the ground.

Given the fundamental nature of bipedal locomotion to the function of humans, we will examine various morphologic changes that occurred throughout human evolution and that promoted the bodies’ ability to perform this act with great efficiency compared to other species. Again, it is far beyond the scope of this chapter to examine all relevant biologic, environmental, and cultural happenings that helped “shape” human beings. Fossil records show the appearance of five key milestones that occurred during the ape-human bifurcation that are worth discussing114 (see Fig. 39.18):

  • Springy arches in foot

  • Big toe function for propulsion

  • Lateral-facing pelvis with expansion of gluteal region

  • Nuchal line thickening

  • An arched lumbar spine

Structure and function are intimately related. The morphologic changes listed here coincide with functional and capacity changes that allowed for a different output between apes and humans. It is of note that these structural changes and the evolution of habitual bipedalism did not occur overnight and did not require a radical transformation of the body. Although few mammals habitually stand and walk on two legs, the anatomic features that make hominins effective bipeds are actually just modest shifts that were evidently subject to natural selection.114 It is easy to imagine how these adaptations are beneficial (and necessary) in our modern world; however, there was a trade-off for each of these changes in the ancient world. For example, changes in foot and big toe structure may help promote a habitual bipedal gait to cover greater distances searching for food but simultaneously they would make an individual less proficient at climbing to escape predators or access food high in the trees.

Springy Arches in Foot

Humans typically strike the ground with the heel first and then, as the rest of the foot contacts the ground, the arch stiffens, allowing the body to project forward and upward at the end of the stance phase, or the “toe off” phase.114 The shape of the foot’s arches is created by the bones and supported by the ligaments and muscles much like cables in a suspension bridge (see Figs. 39.19, 39.20, 39.21, 39.22). These “cables” can achieve various degrees of tightness or springiness depending on the demands placed upon them. Chimpanzees and apes lack an arch, preventing them from pushing off against a stiffened foot.114

This “springiness” is something that we take for granted as humans but can be appreciated by watching the difference in a chimpanzee’s gait pattern to that of model humans.

Figure 39.19 Springiness of the foot arches. © BodyScientific. Stoxen J. The Human Spring Approach to Thoracic Outlet Syndrome. Chicago, IL: Masters Academy Publishing; 2018.

Figure 39.20 Arches of the foot.

Figure 39.21 How arches are used in foot loading.

Figure 39.22 Transverse arch.

Figure 39.23 Big toe orientation and arch formation.

Big Toe Oriented Forward and Shortened

The shortened and forward-oriented big toe in the human foot is more suitable for propulsion compared to those of apes and chimps (see Fig. 39.23).114 In addition, the surfaces of the joints between the toes and the rest of the foot in humans are more rounded and point slightly upward, helping us bend our toes at an extreme angle (hyperextend) when we push off.114 This adaptation pairs with the springy arches to allow for a more efficient and effective form of forward locomotion.

As demonstrated in Figures 39.24, 39.25, 39.26, 39.27, this adaptation allows humans to have a more tightly controlled center of gravity (COG) through a combination of big toe extension, ankle mobility, and torso stiffening rather than an inefficient hip flexion strategy.

Figure 39.24 Center of mass shifts.

Figure 39.25A Proper positioning for push off and forward lean.

Figure 39.25B Improper positioning.

Figure 39.26 Examples of push off and forward lean.

Figure 39.27 Examples of push off and forward lean.

Lateral Facing Pelvis With Expansion of Gluteal Area

The lateral facing pelvis (as opposed to the backward facing ilium in apes) and broader surface area for attachment of pelvis and hip musculature of humans allow for increased efficiency when walking compared to that of chimps (see Figs. 39.28 and 39.29B).129 As noted earlier from Lieberman, “Chimps have shorter legs, they sway from side to side, and they always walk with bent hips and knees. Apes hips sway side to side like a drunkard.”114 This sideways orientation was a crucial adaptation for bipedalism because it allows the lateral hip musculature to effectively stabilize the torso over the stance leg during gait. A larger hip joint, long neck, and wider upper shaft also assist in this action. When a chimpanzee walks on two feet, its legs are spread far apart and there is a significant side to side swaying of their torso. Much of their energy is
spent moving side to side as opposed to the forward motion that occurs in humans.129

Figure 39.28 Difference in pelvic shapes between chimpanzee (A) and modern human (B).

Figure 39.29A Ape pelvic gluteal muscles. Reprinted with permission from Bramble DM, Lieberman DE. Endurance running and he evolution of Homo. Nature. 2004;432:345-352.

Figure 39.29B Modern human pelvic gluteal muscles. Reprinted with permission from Bramble DM, Lieberman DE. Endurance running and he evolution of Homo. Nature. 2004;432:345-352.

Nuchal Line Thickening

The nuchal lines are four transverse curved ridges on the external surface of the occipital bone (see Figs. 39.30, 39.31, 39.32, 39.33, 39.34, 39.35).130 These lines serve as attachment points to a variety of muscles arising from the spine that help to stabilize and maintain posture of the head and neck. Broadly speaking, these muscles belong to a group called the “posterior chain” muscles, which also include the hamstrings, gluteus maximus, and erector spinae.

Thickening of these ridges allows for increased surface area of muscle attachment and, therefore, increased head and neck stability during forward propulsion. This is especially important during the action of running as it typically occurs with a forward lean where increased head and neck stability is required. “Bobbling” of the head back and forth would be an inefficient (and dizzying) locomotion strategy.114

Figure 39.30 Maintenance of head posture while walking. Reprinted with permission from Bramble DM, Lieberman DE. Endurance running and he evolution of Homo. Nature. 2004;432:345-352.

Figure 39.31 Maintenance of head posture while running. Reprinted with permission from Bramble DM, Lieberman DE. Endurance running and he evolution of Homo. Nature. 2004;432:345-352.

Figure 39.32 Larger brain size.

Figure 39.33 Superficial back line. Bucci C. Condition-Specific Massage Therapy. Baltimo, MD: Lippincott Williams & Wilkins; 2012.

Figure 39.34 Difference in skull shapes among chimpanzee (A), hominid (B), and human (C).

Figure 39.35 Lack of head bobbing during running.

An Arched Lumbar Spine

Like other quadrupeds, apes have spines that curve gently (the front side is slightly concave), so when they stand upright, their trunks naturally tilt forward (see Figs. 39.36, 39.37, 39.38).114 As a result, the ape’s torso is positioned unstably in front of its hips. In contrast, the human spine has two pairs of curves. The lower, lumbar curve is made possible by having more lumbar vertebrae (apes usually have three or four, whereas humans usually have five), several of which have a wedge shape in which the top and bottom surfaces are not parallel.114 Just as wedge-shaped stones allow architects to construct arched structures like bridges, wedged vertebrae curve the lower spine inward above the pelvis, positioning the torso stably above the hips. Human chest and neck vertebrae create another, gentler curve at the top of the spine, which orients the upper neck downward rather than backward from the skull.

Figure 39.36 Increased lordotic curve during pregnancy. Reprinted by permission from Springer Nature: Whitcome KK, Shapiro LJ, Lieberman DE. Fetal load and the evolution of lumbar lordosis in bipedal hominins. Nature. 2007;450:1075-1078.

One major drawback with being bipedal is coping with pregnancy.114 Pregnant mammals, four-legged or two-legged, have to carry a lot of extra weight not only from the fetus but also from the placenta and extra fluids. By full term, a pregnant human mother’s weight increases typically by at least 7 kg (15 lb). But unlike in quadruped mothers, this extra mass has a tendency to cause her to fall forward because it shifts her COG well in front of the hips and feet. As pregnancy progresses, a woman must counteract the forward shift in her COG, which can lead to hyperlordosis or back muscle fatigue. The hyperlordosis or swayback saves energy, but places extra shearing stresses on the lumbar vertebrae. LBP is thus a common, debilitating problem for human mothers. Yet we can see that natural selection helped hominin mothers cope with this extra load by increasing the number of wedged vertebrae over which females arch their lower spines: three in females versus two in males.131 This extra curving reduces shearing forces in the spine.

Figure 39.37 Female versus male lumbar lordosis.

Figure 39.38 Placement of torso over hips.

There remains a great deal that we don’t know about how these ancient humans and apes stood, walked, and ran because skeletal remains from this period in Africa are sparse. However, the five adaptations discussed here should provide for an appreciation for the millions of years of “selection” through evolution that allows modern humans to function as efficient bipeds. The first bipeds likely didn’t get up on two feet in order to free their hands; instead, they probably became upright in order to forage more efficiently and to reduce the energetic cost of walking. In this respect, bipedalism was probably an expedient adaptation for fruit-loving apes to survive better in more open habitats as Africa’s climate cooled.

Ultimately, being upright, which occurred over 7 million years ago, did not equate to us fully realizing our modern expression as Homo sapiens. Steps such as the development of language needed to occur.

“As far as visually guided pointing is concerned, a lot of animals (primates and non-primates) are able to look where another individual is pointing…. Chimps point at things they want (imperative pointing) but as far as we know, only humans point to share information (declarative pointing)” (Isbell, personal correspondence). “It appears from the evidence that we have now, that declarative pointing evolved sometime after the hominin-chimp/bonobo split that occurred about 6 million years ago.” This, “coincided with the evolution of bipedality but at that time we were not yet ‘Homo sapiens.’ Our particular species didn’t appear until much, much later. When our ancestors started to walk upright, the lineage consisted of the genera Australopithecus and Paranthropus but not Homo.”

A Sample of Assessment Tests


The modern management of neuromusculoskeletal problems focuses on functional reactivation, restoration, and rehabilitation. Structural problems such as herniated discs or arthritis are relevant in a small percentage of cases and are typically coincidental findings. Therefore, the functional assessment has become a pivotal and often misunderstood component in patient care.

The purpose of functional assessment is to identify a patient’s tolerance, competency, and capacity, as well as functional or performance deficits. This is crucial to create a precision program that bridges the gap from what a patient has (current capacity shortfall) to what they need (required capacity or demands). These functional tests do not replace the initial diagnostic triage of patients, but rather complement it. Acute patients typically receive an evaluation to rule out red flags of serious disease (i.e., tumor, infection, fracture, widespread neurologic loss, or rheumatologic disorder) or nerve root compression. Fortunately, serious disease is present in less than 1% of cases and nerve root compression less than 10% of the time. Evidence-based consensus panel guidelines conclude that in over 80% of LBP patients, the exact pain generator cannot be identified and the label “nonspecific or mechanical back pain” is applied. It is precisely because of this situation that the functional assessment is so important. Patients want to know what is causing their pain, and although a functional diagnosis does not pinpoint causality, it does give the clinician essential targets for reactivation as well as providing simple, inexpensive tests that can be used to audit the patient’s progress toward activity-related goals and recovery.

When a report of examination findings is being given to the patient, it is important to offer a concrete plan of action. This must include measurable landmarks even if specific timelines can’t be given. The major types of care offered should be described and the goals specified. Patients are seeking relief of pain and the modern approach is to reduce threat and AI, increase movement competency and confidence, build strength and robustness, and promote adaptability.

Although the specific “functional” needs of individuals vary, the fundamental patterns and movement literacies performed throughout activities of daily living and across a wide range of populations are, therefore, a logical starting point for movement assessment. Three universal buckets according to Nicole Rodriguez (U.C.L.A. lecture 2018) are

  • Triple flexion

  • Triple extension

  • Rotation

Basic patterns we use every day to train people include squat, single leg bias (e.g., lunge), hinge, push, pull, and locomotion (e.g., carry). However, according to Fred Duncan, these are simply means we use to develop biomotor abilities in hopes of improving movement (personal correspondence). In rehabilitation, we use these BTEs daily but, according to Fred Duncan, “I also understand that I don’t have to. I think truly understanding that is every bit as important as having a plug and play program.” For example, a sprinter may benefit from having a stronger squat, but this is certainly not true for ALL sprinters. Many world record holders are not very skilled in the gym. This is a point that should be borne in mind so that we can avoid confirmation bias in our choices of tests and exercises. As Dr Lewit taught, “Don’t be a slave of methods, the methods should serve the goals.”

Additional characteristic functions to be assessed include:

  • triplanar control

  • time under tension

  • landing ability

  • change of direction ability

  • agility

  • balance

  • mobility

  • muscle endurance

  • etc.

Choosing the correct functional tests is an art and a science. For acute patients, identifying the movements or positions that reproduce the patient’s characteristic pain—their MS—is essential on an initial visit. This becomes a key audit tool (e.g., posttreatment check) for adjudicating and legitimizing the treatment or exercise prescription, and thus motivating the patient. Once acute pain settles, a more comprehensive functional assessment evaluating AMC or painless dysfunctions can also be performed. The tests chosen will be based on the functional goals or AIs of the patient, in other words, what activities they want or need to do that they are having difficulty performing.

These tests should not be thought of as a SCREEN. The idea that a set of tests can serve as a screen of one’s risk of injury or poor recovery has been debunked (Bahr). Instead, this is merely a list of options for patient evaluation that can be individualized based on a person’s chief complaint, activity level, and goals or demands. It is recommended that only a few of these be selected in any particular case. One will get a lot more information by assessing certain basic exercises like the bird dog, hip hinge, or shin box, so it is preferred to expose and train the BTEs early in patient care.

Functional Test Menu (See Also Table 38.6 for Atlas of Tests) (See Appendix Form 1)

  • Sit to stand (see Fig. 39.39A) (triple flexion)

  • Single leg balance (see Fig. 39.40A) (triple extension)

  • Reverse lunge (see Fig. 39.41A) (triple flexion)

  • Vele’s lean (see Fig. 39.42A) (triple extension)

  • Janda’s lunge (see Fig. 39.43A) (triple extension)

  • Single leg squat/step down (see Fig. 39.44A and B) (triple flexion)

  • Single leg hop and hold (see Fig. 39.45A) (triple extension and rotation)

  • Wall angel (see Fig. 39.46A) (triple extension)

  • Jack’s test (see Fig. 47A) (triple extension)

  • Side plank endurance (see Fig. 48A) (frontal plane and rotation)

  • Hip abduction (see Fig. 49A) (frontal plane and rotation)

  • Active and/or resisted straight leg raise (SLR; see Fig. 50A) (rotation)

  • Prone stability shear (see Fig. 51A) (triple extension)

  • Deep neck flexor test (see Fig. 52A) (triple flexion and triple extension)

When instructing assessments, it would be prudent to recall Professor Janda’s advice, “During movement pattern testing, minimal verbal cues should be used which test an individual’s habitual way of performing a movement. If the cues are too ‘leading,’ then the test will be of the subject’s ability to learn how to perform the movement correctly, rather than how they are habitually performing it.”132

For each test, the patient’s MS, scored as a 0, and AMC or painless dysfunction, scored as a 1 or a 2, are noted. Because it is advisable when training patients that good form is ensured, certain signs of faulty movement patterns can be looked for during either movement evaluation or training:

  • Postural dysfunction (see Figs. 38.28, 38.29, 38.30, 38.31, 38.32, 38.33, 38.34)

    • Head forward posture

    • Shrugged shoulder

    • Rounded shoulders

    • Winged scapulae

    • Anterior pelvic tilt or lower crossed syndrome (e.g., “open scissors”)

    • Slumped posture

    • Oblique pelvis

    • Valgus knee

  • Faulty breathing (i.e., chest breathing) (see Fig. 38.35)

  • Poor fitness—High-threshold breathing during low-threshold tasks. In other words, getting out of breath easy and taking a long time to recover.

Note: These dysfunctions may also be coincidental findings, be mindful to avoid overdiagnosis, which can be a nocebo.

This section utilizes a consistent format for describing each test:

  • Indications

  • Procedure

  • Scoring

  • Active interventions to consider

1. Sit to Stand


  • Back pain management

Procedure (see Fig. 39.39A):

  • The test is administered using a chair.

  • The subject is instructed not to use the arm rests.

  • If chair is not secure, place it against a wall.

  • Repeat test twice.

Score: (Pass/Fail)

  • Pass/Fail

  • Fail

    • rising up with a slouched posture

    • using hands for assistance

Active interventions to consider:

Chair Squat Test (Modification)


  • Fall risk

  • Balance

  • Frailty prevention


  • The test is administered using a folding chair without arms, with a seat height of 17 inches (43.2 cm). The chair, with rubber tips on the legs, is placed against a wall to prevent it from moving.

  • The subject is seated in the middle of the chair, back straight, feet approximately shoulder width apart and placed on the floor at an angle slightly back from the knees, with one foot slightly in front of the other to help maintain balance. Arms are crossed at the wrists and held against the chest.

  • Demonstrate the task both slowly and quickly.

  • Have the subject practice a repetition or 2 before completing the test.

  • If the subject must use their arms to complete the test, they are scored 0.

  • The subject is encouraged to complete as many full stands as possible within 30 seconds. The subject is instructed to fully sit between each stand.

Score: (Pass/Fail)

  • Pass: Equal to or above normative data for age group

    • Normative data135,136: Age 60 to 64 years—15 to 17 reps; 65 to 69 years—15 to 16 reps; 70 to 74 years—14 to 15 reps; 80 to 84 years—12 to 13 reps; 85 to 89 years—11 reps; 90 to 94 years—9 reps

  • Fail: Less than normative date for age group

Active interventions to consider:

Figure 39.39A Repeated sit-to-stand.

Figure 39.39B Door handle squat.

Figure 39.39C TRX squat.

Figure 39.39D Arm rest squat.

2. Single Leg Balance

(Bohannon et al,137 Maribo et al,138 Byl and Sinnott,139 See Chapter 21)


  • History of ankle sprains

  • Lower extremity pain

  • LBP

  • Poor balance

  • Elderly fall prevention

  • Assess frontal plane control

Procedure (see Fig. 39.40A):

  • Subject stands with arms folded across chest.

  • Part A: Eyes open

    • The subject is instructed to stand on one leg and look straight ahead.

    • Subject chooses preferred one leg stance position, left or right, and the foot of raised leg is at knee height and not allowed to touch stance leg.

    • If they can do 10 seconds eyes open (EO), then continue to Part B.

  • Part B: Eyes closed

    • The subject is instructed to stand on one leg and look straight ahead, focusing on a spot on the wall in front.

    • Now, give instruction: continue balancing and close your eyes (EC).

  • Subject gets up to five tries on each leg.

  • Test ends when:

    • Stance foot hops or twists on floor.

    • Either hand reaches for support.

    • Raised leg foot is put down.

  • Normative data137: Age 20 to 49 years—24 to 28 seconds; 50 to 59 years—21 seconds; 60 to 69 years—10 seconds; 70 to 79 years—4 seconds

Score: (Pass/Fail)

  • 0: pain

  • 1:

    • Less than 10 seconds EO

    • Less than 5 seconds EC

    • Pelvic shift > 1 inch during EO

    • Asymmetry greater than 10%

  • 2:

    • Less than 30 seconds EO

    • Less than 10 seconds EC

    • Medial collapse of the forefoot

  • 3:

    • Greater than 30 seconds EO

    • Greater than 10 seconds EC

Active interventions to consider:

Figure 39.40A Single leg balance with eyes closed.

Figure 39.40B Rocker board training.

Figure 39.40C Wobble board.

Figure 39.40D1 Standing on balance shoes with support.

Figure 39.40D2 Walking with balance shoes.

Figure 39.40E1 Inline walking, start position.

Figure 39.40E2 Inline walking, finish position.

Figure 39.40F Tandem balance.

Figure 39.40G Inline balance.

Figure 39.40H Single leg balance with eyes closed.

Figure 39.40I1 Single leg balance with head extensions, start position.

Figure 39.40I2 Single leg balance with head extensions, finish position.

Figure 39.40J The small foot.

3. Reverse Lunge


  • Leg strength assessment

  • Prevention of frailty

  • Fall prevention

Procedure (see Fig. 39.41A):

  • From a neutral standing position, direct the subject to step backward until they are kneeling on one knee.

  • Return to standing.

  • Repeat on the opposite side.

Score: (Pass/Fail)

  • 0: Pain

  • 1: Unable to perform

  • 2:

    • Front knee passes forward of toes

    • Front knee valgus medial to the great toe

    • Poor hallux extension on the rear foot

  • 3: Able to perform without compensation

Active interventions to consider:


  • Reverse lunge slider (see Fig. 39.41B)

  • Half-kneeling (see Fig. 39.41C)

  • Supported reverse lunge

  • Split stance (see Fig. 39.41D) (front foot elevated, rear foot elevated)


Figure 39.41A Reverse lunge.

Figure 39.41B1 Reverse lunge with slider, start position.

Figure 39.41B2 Reverse lunge with slider, finish position.

Figure 39.41C Half-kneeling stance.

Figure 39.41D1 Split stance, start position.

Figure 39.41D2 Split stance, finish position.

Figure 39.41E1 Deficit lunge, start position.

Figure 39.41E2 Deficit lunge, finish position.

4. Vele’s Forward Lean


  • LBP

  • Assess intrinsic foot activation and sagittal plane motor control

  • Assess ankle dorsiflexion mobility

Procedure (see Fig. 39.42A):

  • Subject begins in a neutral standing posture.

  • Instruct subject to lean forward from the ankles without bending at the waist—“leaning tower” position.

  • Cue subject to keep heels connected to the floor.

Score: (Pass/Fail test)

  • Fail

    • Delayed, absent, or asymmetric gripping of the toes

    • Claw toes (flexion of the interphalangeal joint)

    • Flexion at hips

Active interventions to consider:

Figure 39.42A1 Vele’s lean, start position.

Figure 39.42A2 Vele’s lean, finish position.

Figure 39.42A3 Vele’s lean, poor form—bending at the waist.

Figure 39.42B Vele’s lean with lateral lean.

Figure 39.42C Trust fall.

Figure 39.42D Wall drill.

Figure 39.42E1 Sled pull, start position.

Figure 39.42E2 Sled pull, finish position.

Figure 39.42F Sled push.

Figure 39.42G1 2 feet saw plank, start position.

Figure 39.42G2 2 feet saw plank, finish position.

5. Janda’s Lunge


  • LBP

  • Knee pain

  • Assess sagittal plane knee and lumbopelvic motor control

Procedure (see Fig. 39.43A):

  • Subject begins in a neutral standing position.

  • Cue to slowly lean forward from the ankles without bending at the waist.

  • Next, give instruction: when the heels begin to lift, step forward and “stick” landing.

  • Maintain a forward lean.

  • Repeat on opposite side.

Score: (Pass/Fail)

  • Knee passes forward of toes

  • Knee valgus inside the great toe

  • Trunk flexion

  • Loss of “leaning tower”

Active interventions to consider:

Figure 39.43A1 Lunge.

Figure 39.43A2 Janda’s lunge, incorrect form—anterior translation of knee.

6. Single Leg Squat/Step Down

(See Chapter 12, Räisänen et al140; Numata et al141; Liebenson142; Hewett and Myers143; Hewett et al144; Hewett et al145)


  • Lower extremity pain

  • LBP

  • Assess triplanar control

Procedure (see Fig. 39.44A and B):

  • Subject begins by standing on 1 leg.

  • Instruct subject to perform a mini-squat to 30 degrees of knee flexion.

  • Alternatively, perform a step down from an 8 inch or 20 cm height step by lowering one leg slowly down until the heel lightly taps the ground.

  • Repeat a few times.

Score: (Pass/Fail)


  • Unable to balance on 1 leg

  • Unable to squat to 30 degrees of knee flexion or in the step down to lightly tap the heel to the ground

  • Knee valgus inside the great toe

Active interventions to consider:

Figure 39.44A Single leg squat.

Figure 39.44B Step down.

Figure 39.44C1 Single leg box squat, start position.

Figure 39.44C2 Single leg box squat, finish position.

Figure 39.44D Lateral wall drill.

Figure 39.44E Lateral acceleration drill.

Figure 39.44F1 Peterson step down, start position.

Figure 39.44F2 Peterson step down, finish position.

Figure 39.44G Step-ups.

Figure 39.44H1 1 leg gluteal bridge, start position.

Figure 39.44H2 1 leg gluteal bridge, finish position.

Figure 39.44I1 Reverse lunge slider with heavy band pulling medially, start position.

Figure 39.44I2 Reverse lunge slider with heavy band pulling medially, finish position.

Figure 39.44I3 Reverse lunge slider with heavy band pulling anteriorly.

Figure 39.44J1 1 leg Romanian deadlift (RDL) with support, start position.

Figure 39.44J2 1 leg RDL with support, finish position.

7. Single Leg Hop and Hold143


  • Lower extremity pain

  • LBP

  • Assess triplanar control

  • Assess energy storage and release


  • Acute hip/knee/ankle trauma

  • Instablity

  • Unable to perform two/1 leg squat; two/1 leg hop

Procedure (see Fig. 39.45A):

  • Before initiating this challenging test, attempt submaximal two leg and single leg broad jumps.

  • The starting position for this jump is a semicrouched position on a single leg.

  • The subject’s arms should be fully extended behind them at the shoulder.

  • The jump is initiated by swinging the arms forward while simultaneously extending at the hip and knee.

  • The subject is instructed to land on the jumping leg and hold the landing with a deep knee bend for a minimum of 3 seconds.

  • Begin with submaximal effort and repeat with increasing the distance as the athlete improves their ability to stick and hold final landing.

Score: (Pass/Fail)


Trunk Dominance

  • Center of mass (COM) forward of base support

Leg Dominance

  • Marked asymmetry side to side

Quadriceps Dominance

  • Failure to hip hinge

Ligament Dominance

  • Increased knee valgus with knee translating medial to great toe

Active interventions to consider:

Figure 39.45A Single leg hop and hold.

Figure 39.45B1 Energy storage and release—landing on 1 foot, start position.

Figure 39.45B2 Energy storage and release—landing on 1 foot, finish position.

Figure 39.45C Single leg 4 square hop.

8. The Wall Angel146


  • LBP

  • Neck pain

  • Upper extremity pain

  • Thoracic, rib, and shoulder mobility

  • Assessment of upright posture

  • Assess sagittal plane mobility and posture

Procedure (see Fig. 39.46A):

  • Subject stands near the wall with gluteal muscles, thoracic spine, and head touching the wall with a horizontal gaze.

  • Instruct subject to flex elbows to 90 degrees, abduct shoulders to shoulder height, and externally rotate the arm to bring all 10 fingers into contact with the wall.

  • Then ask the patient to move the thoracolumbar (T/L) junction toward the wall.

Score: (Pass/Fail)


  • Chin poke or head not able to maintain contact with the wall with horizontal gaze

  • All 10 fingers not touching the wall

  • Wrist >1 cm distance away from wall

  • T/L junction is not able to move toward the wall

  • Utilization of posterior pelvic tilt strategy to approximate T/L junction to the wall rather than lowering ribs

Active interventions to consider:

Figure 39.46A Wall angel.

Figure 39.46B1 Cookband, start position.

Figure 39.46B2 Cookband, finish position.

Figure 39.46C1 Kettlebell overhead, start position.

Figure 39.46C2 Kettlebell overhead, finish position.

9. Jack’s Test147


  • Assess 1st metatarsophalangeal (MTP) mobility

Procedure (see Fig. 39.47A):

  • Subject begins seated or standing.

  • Assess hallux dorsiflexion passive range of motion (PROM).

Score: (Pass/Fail)

  • Fail

    • No data on what a normal ROM is for this test

    • Greater than 20% asymmetry is key

    • A general guideline is

      • ▪ hallux dorsiflexion less than 40 PROM in standing position

      • ▪ hallux dorsiflexion less than 70 PROM in seated position

Active interventions to consider:

Figure 39.47A Jack’s test. Adapted from Fig 5.21, Michaud TC. Human Locomotion: The Conservative Management of Gait-related Disorders. Newton, MA: Newton Biomechanics; 2011.

Figure 39.47B Lacrosse ball.

Figure 39.47C Toe sit.

Figure 39.47D Cowboy sit.

10. Side Plank Endurance148


  • LBP

  • Endurance

  • Assess frontal plane control and core activation

Procedure (see Fig. 39.48A):

  • Patient begins on their side, places top foot in front of their bottom foot, and supports themselves up on their elbow.

  • Instruct patient to raise up as high as possible so long as the spine is not side bending with convexity toward the ceiling. Only feet and forearm/hand are on the floor. Upper arm can rest along the side of the body or against the chest.

  • When patient loses height, cue them to raise up again. The second time the pelvis drops from its peak height is recorded as test end.

  • Perform test on each side.

Normative data148

  • <45 seconds = dysfunction

  • side to side asymmetry <5%

Score: (Pass/Fail)


  • Less than 45 seconds

  • Asymmetry greater than 5%

Active interventions to consider:



Figure 39.48A Side plank endurance.

Figure 39.48B Front plank.

Figure 39.48C1 Side bridge, start position.

Figure 39.48C2 Side bridge, finish position.

Figure 39.48D1 Plank roll, start position.

Figure 39.48D2 Plank roll, intermediate position.

Figure 39.48D3 Plank roll, finish position.

Figure 39.48E Copenhagen adductor.

Figure 39.48F Crossover sled drill.

11. Janda’s Hip Abduction Test

(Chapter 11, Lewit149; Nelson-Wong et al83)


  • Ankle sprain

  • Iliotibial band syndrome

  • Patellofemoral pain syndrome

  • Lower extremity pain

  • LBP

  • Assess frontal plane control

Procedure (see Fig. 39.49A):

Part A

  • Subject is side lying with lower leg flexed at hip and knee.

  • Stack the pelvis perpendicular to the table.

  • Instruct the subject to slowly raise leg straight up to 40 to 45 degrees of abduction.

  • If able to maintain unassisted, continue to Part B.

Part B

  • Guide upper leg to 40 to 45 degrees of pure hip abduction if not already there.

  • Perform resisted hip abduction with hand contact just below the knee.

Score: (Pass/Fail)


  • Can’t abduct 40 degrees

  • Manual muscle test at 40 degrees abduction less than 4+/5

  • Compensatory hip flexion or pelvic rotation

  • Lack of endurance

  • Significant cephalad shift of the pelvis (e.g., hip hike)

Active interventions to consider:

  • Baby get up (see Fig. 39.49B)

  • Facilitate with manual resistance (see Fig. 39.49C)

  • Gluteal bridges (see Fig. 39.44H)

  • Also see Frontal plane trainable menu on page 1084

Figure 39.49A Hip abduction.

Figure 39.49B1 Baby get up, start position.

Figure 39.49B2 Baby get up, finish position.

Figure 39.49C Hip abduction with manual resistance.

12. The Active Straight Leg Raise (ASLR)150,151


  • LBP

  • Posterior pelvic pain

  • Assess core control of transverse and sagittal plane

Procedure (see Fig. 39.50A):

  • Part A: ASLR

    • Subject is supine.

    • Instruct subject to perform a straight leg raise 20 cm up from the table.

    • If able to maintain unassisted, continue to Part B.

  • Part B: Resisted Straight Leg Raise (RSLR)

    • Perform resisted strength test (with leg raised 20 cm from table) with hand contact just above the ankle.

    • Note: Patient may place hands under small of the back in order to palpate loss of pressure and trunk rotation with their hands.

Score: (Pass/Fail)


  • Asymmetric or significant trunk rotation when leg held at 20 cm flexion during ASLR or RSLR

  • Manual muscle test grade less than 4-/5 during RSLR

Active interventions to consider:

Figure 39.50A Active and/or resisted straight leg raise.

Figure 39.50B Postural Restoration Institute considerations.

13. Prone Stability Shear Test152


  • LBP

  • To identify a patient who is likely to improve with isometric torso exercise.

Procedure (see Fig. 39.51A):

  • Subject is prone with hips at edge of table and feet dangling off table, torso and upper body supported.

  • Clinician performs posterior to anterior compressions over the spinous process.

  • If painful, then have subject raise legs up and recheck sensitivity.

Score: (Pass/Fail)

  • Pass: The patient feels pain when the feet are on the ground and no or less pain with the feet in the air

  • Fail: No change in symptoms

  • Note:

  • Patients who pass this test are expected to respond well to an isometric trunk exercise program.

  • This test can be used to reassure a fearful or apprehensive patient that strengthening/stability will help their symptoms.

  • Failure of symptoms to improve suggests that other interventions are needed to “calm things down” before the isometric trunk exercises are used to begin the process of “building them up.”

Active interventions to consider:

Figure 39.51A Prone stability shear.

Figure 39.51B1 Quad leg reach.

Figure 39.51B2 Quad opposite arm and leg reach.

Figure 39.51B3 Poor form, lumbar hyperextension and chin poking.

Figure 39.51B4 Rotation controlled.

Figure 39.51B5 Overrotated.

Figure 39.51C1 Beginner back extension exercise.

Figure 39.51C2 Intermediate back extension exercise.

Figure 39.51C3 Advanced back extension exercise.

Figure 39.51D Superman on ball.

14. Deep Neck Flexor Test

(Chapter 11; Jull et al153)


  • Neck pain

  • Headache

  • Whiplash syndromes

  • To identify coordination during head/neck flexion

Procedure (see Fig. 39.52A):

  • Subject lays supine.

  • Slowly raise head up from table toward chest.

Score: (Pass/Fail)


  • Chin protrusion

  • Shaking

  • Poor endurance

  • Visible overactivity of the sternocleidomastoid musculature

Active interventions to consider:

  • C0-C1 flexion*

  • Prone sphinx (see Fig. 39.52B)

  • Quadruped (see Fig. 39.52C)

  • Push-up position (high plank) (see Fig. 39.52D)

  • Vocal training (ahh, nnn, hmm, tss)

  • See also Wall angel trainable menu on page 1016

*Note: C0-C1 is basically like nodding, yes. It is not a chin tuck where the patient is making a double chin.

Figure 39.52A Janda’s neck flexion test.

Figure 39.52B1 Prone sphinx, start position.

Figure 39.52B2 Prone sphinx, finish position.

Figure 39.52B3 Prone sphinx, incorrect form—neck crease.

Figure 39.52B4 Prone sphinx, correct form.

Figure 39.52C Quadruped.

Figure 39.52D Push-up position.

Movement Preparation

The MP can be thought of as a dynamic “warm-up.” It prepares a person to train, perform a recreational activity, or participate in competitive sport. It can vary from just a few minutes to as long as 40 minutes depending on your goals. The purpose is to establish “readiness” for more robust physical demands. It also is a motor learning process, and because every exercise is a test it is thus an evaluation of one’s movement competency.

See Table 38.8 for a concise version of our MP. This section shows a more comprehensive menu highlighting more options. The MP is a cornerstone of foundational movement literacies—ABCs of agility, balance, and coordination—that can be used for many purposes besides a dynamic “warm-up” such as:

  • during the recovery stage on a low intensity or deload day;

  • to calm things down before building them up in rehab;

  • during interval training to reestablish a normal resting heart rate after the high-intensity interval;

  • to potentiate bigger lifts.

Movement Prep Atlas (See Appendix Form 2)

1. Sensory Afferent

According to Professor Vladimir Janda, it is recommended that normalization of afferent inputs into the sensory-motor axis is a prerequisite for facilitation of optimal movement patterns (see Chapter 21). The feet play a special role in this regard as they are our main connection with our environment and are responsible for a high proportion of expected information in the sensory cortex or homunculus. Modern society ignores the feet (see Evolution section) and in fact creates a “dead” foot by virtue of the fact that:

  • We sit so much

  • Our feet are entombed in shoes

  • When we do walk it is typically on flat or cushioned surfaces

Philip Beach, D.O. speaks of the evolutionary role of support from different body parts, in particular, the feet, in order to “tune” the function of our locomotor system.154 The lack of movement variability and the precipitous rise of sedentary postures have resulted in an increase in evolutionary mismatch conditions such as LBP, heart disease, fallen arches, obesity.114 Lieberman,114 a Harvard evolutionary biologist, mentions that hominoids are over 7 million years old, but it is only within the last 100,000 years that we even began wearing moccasins. We are in fact suffering from sensory blindness because of the lack of sensory input from the periphery of the body (called deafferentiation).

Figure 39.53A Lacrosse ball.

Figure 39.53B Toe sit.

Figure 39.53C Cowboy sit.

2. Physiologic

Once the sensory system is woken up with work on the sole of the foot, the next step is a physiologic priming via increasing heart rate, core body temperature, and shifting respiration from low to high threshold. This is the only true “warm up” in our MP. The individual should experience a faster and deeper breathing pattern, slight perspiration, and an elevated heart rate. Each of these is an objective indicator of the physiologic priming needed to prepare a person for more robust training. In addition, these preps are primal, so by using the upper quarter in a closed chain they are excellent for arm health and to promote afferents from the palms of the hands to the scapular area.

Figure 39.54A1 Beast crawl, start position.

Figure 39.54A2 Beast crawl, intermediate position.

Figure 39.54A3 Beast crawl, finish position.

Figure 39.54B1 Torsion buttress.

Figure 39.54B2 Torsion buttress, poor form—twisting.

Figure 39.54B3 Torsion buttress, poor form—twisting.

Figure 39.54C1 Plank to push-up, start position.

Figure 39.54C2 Plank to push-up, intermediate position.

Figure 39.54C3 Plank to push-up, finish position.

3. Active Mobility

The next logical step in the MP is to explore ROM of key structures such as ankle, hip, and thoracic spine. This can be done passively, but we prefer an active approach to orient awareness of positional control as a prelude adding load and speed.

Figure 39.55A1 Shinbox, right.

Figure 39.55A2 Shinbox, left.

Figure 39.55B1 Shinbox get up, start position.

Figure 39.55B2 Shinbox get up, intermediate position.

Figure 39.55B3 Shinbox get up, intermediate position.

Figure 39.55B4 Shinbox get up, finish position.

Figure 39.55C1 Shinbox with passive hip internal rotation.

Figure 39.55C2 Shinbox with active hip internal rotation.

Figure 39.55D1 Granby roll, start position.

Figure 39.55D2 Granby roll, intermediate position.

Figure 39.55D3 Granby roll, finish position.

Figure 39.55E1 Tactical frog, start position.

Figure 39.55E2 Tactical frog, finish position.

Figure 39.55F1 Quadruped hip internal rotation, start position.

Figure 39.55F2 Quadruped hip internal rotation, intermediate position.

Figure 39.55F3 Quadruped hip internal rotation, finish position.

Figure 39.55G1 Supported piriformis stretch.

Figure 39.55G2 Supine piriformis stretch.

Figure 39.55H1 Half-kneeling halo, start position.

Figure 39.55H2 Half-kneeling halo, intermediate position.

Figure 39.55H3 Half-kneeling halo, finish position.

Figure 39.55I1 Inline half-kneeling halo, start position.

Figure 39.55I2 Inline 1/2 kneeling halo, finish position.

Figure 39.55J1 Standing halos with shoulder Rok, start position.

Figure 39.55J2 Standing halos with shoulder Rok, intermediate position.

Figure 39.55J3 Standing halos with shoulder Rok, finish position.

Figure 39.55J4 Tall kneeling halos with shoulder Rok, start position.

Figure 39.55J5 Tall kneeling halos with shoulder Rok, intermediate position.

Figure 39.55J6 Tall kneeling halos with shoulder Rok, finish position.

Figure 39.55K1 Sotts press, start position.

Figure 39.55K2 Sotts press, finish position.

Figure 39.55L Cat cow.

Figure 39.55M1 Jiri sphinx, start position.

Figure 39.55M2 Jiri sphinx, finish position.

Figure 39.55N T4 rotation.

Figure 39.55O Jerzy T4 extension.

Figure 39.55P1 Cressey T-spine extension, start position.

Figure 39.55P2 Cressey T-spine extension, finish position.

Figure 39.55Q1 Vertical foam roller arms by side.

Figure 39.55Q2 Vertical foam roller arms over head.

Figure 39.55R1 Horizontal foam roller supine.

Figure 39.55R2 Horizontal foam roller prone, start position.

Figure 39.55R3 Horizontal foam roller prone, finish position.

Figure 39.55S1 Arm bar, start position.

Figure 39.55S2 Arm bar, finish position.

Figure 39.55T Deep squat.

Figure 39.55U1 Anterior balance reach.

Figure 39.55U2 Lateral balance reach.

Figure 39.55U3 Posterior balance reach.

4. Pillar Preparation

The functional assessment often reveals a lack of the ability to stiffen torso efficiently. Gluteal and abdominal muscle activation is a basic MP to accompany ADLs, sport, fitness, or load. Another common finding is quadriceps dominance, and thus posterior chain facilitation is necessary to create not only improved kinetic chain function for areas such as the knee or lumbar spine, but also to enhance performance such as in overhead sports or sprinting (see Chapter 18). Similarly, various abdominal exercise routines (see Chapters 19 and 32) can be helpful to create a torso stiffness for either the arms or legs to generate or release power.

When considered from an athletic perspective such as sprinting, kicking a soccer ball, throwing a javelin, generating rotatory power during the golf swing, balancing on a surfboard when navigating a wave, striking a ball in water polo, accepting a violent hit in American football, it is apparent that the torso is a key link in the kinetic chain.

Some schools such as Dynamic Neuromuscular Stabilization (DNS) (see Chapter 31) or PRI speak at length about the role of the pillar, cylinder, rib cage, diaphragm, pelvic floor, etc. Pilates, the Queensland group of Hodges & Richardson, and Professor Stuart McGill all emphasize the importance of the abdominal wall.152,155,156

Professor Janda described a lower crossed syndrome (see Chapter 11) wherein abdominals and gluteals are inhibited because of our modern, sedentary lifestyle.157,158 This is combined with a faulty breathing pattern as secondary muscles of respiration such as the scalenes substitute for the diaphragm because of the effects of the slumped, sitting posture.159 Cumpelik (see Chapter 30) describes how “aplomb” is gained by utilization of support (“barre”) while developing optimal verticalization of posture in preparation of and during forward locomotion challenges.

  • Gluteals

    • 2 and 1 leg gluteal bridge (see Fig. 39.56A and B)

    • 2 and 1 leg gluteal bridge with ball (see Fig. 39.56C and D)

    • 2 and 1 leg hamstring curl (see Fig. 39.56E and F)

    • Functional clamshell (see Fig. 39.56G)

    • Monster walk (see Fig. 39.56H)

    • Split stance with and without weight (see Fig. 39.56I and J)

    • Kickstand with and without weight (see Fig. 39.56K and L)

    • Lateral band walk (see Fig. 39.56M)

    • Hip airplane (see Fig. 39.56N)

    • Wall ball (see Fig. 39.56O)

    • VipR forward lean (see Fig. 39.56P)

    • VipR lateral shift (see Fig. 39.56Q)

      Figure 39.56A1 2 leg gluteal bridge, start position.

      Figure 39.56A2 2 leg gluteal bridge, finish position.

      Figure 39.56B1 1 leg gluteal bridge, start position.

      Figure 39.56B2 1 leg gluteal bridge, finish position.

      Figure 39.56C1 2 leg gluteal bridge with ball, start position.

      Figure 39.56C2 2 leg gluteal bridge with ball, finish position.

      Figure 39.56D1 1 leg gluteal bridge with ball, start position.

      Figure 39.56D2 1 leg gluteal bridge with ball, finish position.

      Figure 39.56E1 2 leg hamstring curl, start position.

      Figure 39.56E2 2 leg hamstring curl, finish position.

      Figure 39.56F1 1 leg hamstring curl, start position.

      Figure 39.56F2 1 leg hamstring curl, finish position.

      Figure 39.56G1 Functional clamshell, start position.

      Figure 39.56G2 Functional clamshell, finish position.

      Figure 39.56H1 Monster walk, start position.

      Figure 39.56H2 Monster walk, finish position.

      Figure 39.56I1 Split stance, start position.

      Figure 39.56I2 Split stance, finish position.

      Figure 39.56J Kickstand position.

      Figure 39.56K1 Split stance with weight, start position.

      Figure 39.56K2 Split stance with weight, finish position.

      Figure 39.56L Kickstand position with weight.

      Figure 39.56M1 Lateral band walk, start position.

      Figure 39.56M2 Lateral band walk, intermediate position 1.

      Figure 39.56M3 Lateral band walk, intermediate position 2.

      Figure 39.56M4 Lateral band walk, finish position.

      Figure 39.56N Hip airplane.

      Figure 39.56O1 Wall ball, start position.

      Figure 39.56O2 Wall ball, finish position.

      Figure 39.56P1 VipR forward lean, start position.

      Figure 39.56P2 VipR forward lean, finish position.

      Figure 39.56Q1 VipR lateral shift, start position.

      Figure 39.56Q2 VipR lateral shift, finish position.

      Figure 39.56Q3 VipR lateral shift with kickstand position.

  • Core

Figure 39.57A1 Cookband, start position.

Figure 39.57A2 Cookband, finish position.

Figure 39.57B1 Cookband in hollow body position, start position.

Figure 39.57B2 Cookband in hollow body position, finish position.

Figure 39.57C1 Kettlebell overhead, start position.

Figure 39.57C2 Kettlebell overhead, finish position.

Figure 39.57D1 Kettlebell overhead in hollow body position, start position.

Figure 39.57D2 Kettlebell overhead in hollow body position, finish position.

Figure 39.57E1 Bug off wall, start position.

Figure 39.57E2 Bug off wall, finish position.

Figure 39.57F1 Plank roll, start position.

Figure 39.57F2 Plank roll, intermediate position.

Figure 39.57F3 Plank roll, finish position.

Figure 39.57F4 Plank roll, poor form—twisting.

Figure 39.57F5 Plank roll, poor form—shoulder-pelvis disassociation.

Figure 39.57F6 Plank roll, proper form.

Figure 39.57G1 Front plank lift off, start position.

Figure 39.57G2 Front plank lift off, finish position.

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Apr 17, 2020 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on A Clinical Framework Utilizing a Precision Approach

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