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Lower Extremity Dysfunction (LED): Predictive Model of Lower Extremity Movement Impairment Audio

Predictive Model of Lower Extremity Dysfunction (LED): Signs of lower extremity/lower body postural dysfunction, muscle, joint, fascia, nervous system, neuromuscular recruitment, subsystems, and core muscle contribution. Exercise selection related to pronation distortion syndrome, feet flatten, forward lean, and feet turn out.

Lower Extremity Dysfunction (LED): Predictive Model of Lower Extremity Movement Impairment

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is an edit and update of previous postural dysfunction models (e.g. lower body posture, lower-crossed syndrome, pronation distortion, functional knee valgus, etc.). It is important to recognize that in these models the term "posture" is being used as an analogy for "ideal alignment". Similarly, when movement professionals refer to lower body posture, good posture, poor posture, better posture, etc. they are referring to this analogy of ideal alignment; not the rigid positioning implied by the colloquial use of the term "posture."

Postural dysfunction and movement impairment syndromes are likely the beginning of "modeling". Modeling has significant potential to aid in refining clinical decision-making, intervention selection, program design, and improve the reliability and effect size of outcomes. Models are especially conducive for assisting in interpreting multi-variant problems, which is how all clients and patients present. The 

 recommends that all sports medicine professionals (personal trainers, fitness instructors, physical therapists, massage therapists, chiropractors, occupational therapists, athletic trainers, etc.) consider these models as an aid in refining decision-making in practice.

Lumbo Pelvic Hip Complex Dysfunction (LPHCD)

 Arthro- and osteo-kinematics alignment maintained by optimal myofascial activity and length, as a result of sensation, integration, and activation by the nervous system - both statically and dynamically.

 The absence of ideal posture as a result of maladaptation by one or multiple tissues within the human movement system.

Modeling patterns of movement impairment correlated with orthopedic dysfunction, based on all available evidence, with the intent of predicting best-practice assessments and techniques, to optimize measured outcomes.

Myofascial Synergies (Altered Recruitment)

Excessive lordosis (Anterior pelvic tilt)

Hip Internal Rotation at 90 Degrees of Hip Flexion

Hip External Rotation at 90 Degrees of Hip Flexion

Knee Extension with Hip Flexion (Hamstring Length

Correlated Injuries, Pathologies, and Pain

The Lower Extremity Dysfunction (LED) model is constructed based on research demonstrating the maladaptive alterations of tissues and motion associated with common impairments of the human movement system. Creating a list of these impairments adds to the definition of the LED model, as the model itself could be defined as the expected maladaptive changes to arise from those impairments.

Medial tibial stress syndrome (24, 34, 44)

Ankle Sprain (Inversion sprain) (62, 75, 123-124, 195, 198 -199, 203 - 204, 207, 211-212)

Ankle instability (19, 34, 71 - 74, 126, 196-197, 200 -202, 205-206, 208-210, 213, 218)

Achilles tendinopathy (31, 34, 42, 44, 156, 159-167)

Tibialis posterior tendinopathy (36 - 39, 110, 115-117, 121

Plantar fasciitis (plantar heel pain,) (43, 69, 111, 153-158)

Anterior cruciate ligament injury (16, 230, 234)

Functional valgus (16 - 18, 23, 26-29, 234)

Knee pain (patellofemoral pain syndrome, jumper's knee ) (46, 48 - 51, 53-54,56, 58-59, 93, 102, 170, 225, 234-236)

Lateral knee pain (iliotibial band syndrome, runner's knee) (172, 215-216)

Proximal tibiofibular joint pathology (215-217)

Tibiofibular joint subluxation/dislocation (218-222)

Femoral acetabular impingement (FAI) (238)

Course Description: Lower Extremity Dysfunction (LED)

For an introduction to Postural Dysfunction and Movement Impairment please refer to:

Introduction to Postural Dysfunction and Movement Impairment

“Lower Extremity Dysfunction (LED)" is a purposely chosen title for the impairment discussed in this article. By naming this model after body segment the risk is reduced that the title itself will imply a certain set of altered osteokinematic and arthrokinematic motions, changes in muscle activity, fascial dysfunction/loss of extensibility, and/or changes in sensation, perception, organization, and motor unit recruitment via the central nervous system. Common compensation patterns leading to LED have been previously described as “pronation" or "pronation dysfunction" (1-6). It is my opinion, these labels may be misleading because they imply a poorly defined set of joint motions. For example, pronation has been used to describe the motion of the ankle, the motion of the forefoot, or haphazardly as a synonym for excessive eversion. The most common use of the term "pronation" implies a combination of joint actions that occur around the oblique axis of the 

 - dorsiflexion, abduction, and eversion.

 dorsiflexion are common findings in those exhibiting lower extremity impairment. If we continue to use a title for this model that implies a specific set of motions (e.g. "pronation" or "pronation dysfunction"), does it describe motions that are excessive, restricted, both, and if both, how is the human movement professional expected to differentiate? Now, consider a model described by body segment. The model may evolve without influence from the label used to describe it. The model may continue to evolve with ever-increasing detail and accuracy as new theoretical constructs, research, techniques, and outcome measures increase our knowledge of impairment for that segment.

LED is limited to common impairments of the 

ankle (and proximal and distal tibiofibular joints respectively)

. It should be noted that this model purposely excludes the foot, despite evidence that LED may result in, or result from altered motion of the foot. The foot will be covered in a separate article for reasons related to education and practice. First, with respect to education, it is easier to retain, comprehend, and practice this information if the lower extremity and foot are initially treated as separate segments. Second, whereas LED may be successfully, and nearly comprehensively addressed using self-administered techniques, comprehensive intervention for foot dysfunction seems to necessitate certain manual techniques. This implies that all human movement professionals may have success addressing LED, whereas foot dysfunction should likely be addressed by licensed professionals whose scope includes joint mobilizations. The line separating the two dysfunctions is the transverse tarsal joint. That is to say that this model does not describe dysfunctional joint motion more distal than the talus and calcaneus.

Introduction

Osteokinematic Dysfunction

Muscle tissue

Muscular Dysfunction

Fascia

Fascial Dysfunction

Myofascial Synergies (Subsystems)

Arthrokinematic Dysfunctions

Summary of Model

The first issue with this model is attempting to identify how pronation and supination would affect muscle length and activity. There are very few “true pronators” and “true supinators” of the ankle. If we used these joint actions alone, our analysis would exclude the gross majority of structures crossing the ankle. For this reason, we have broken down the complex actions of pronation and supination into their component joint actions. Pronation is comprised of plantar flexion, eversion, and abduction; however, abduction has been removed from the graph below, as the muscles that contribute to abduction would also be evertors. Supination is comprised of dorsiflexion, inversion, and adduction; however, adduction has been removed from the graph below, as the muscle that contributes to adduction would also be invertors.

The second issue with this model is the number of muscles that have been listed on both the short and long sides of the graph (in bold). Since a muscle cannot be both shortened and lengthened around the same joint this represents an incongruity; at the very least it represents a point of confusion and possibly conflicting ideas about optimal intervention. If a graph exhibits only a few muscles that appear on both sides we may be able to “label" the muscles as “long/over-active” - a common state of muscles acting as 

, or “short/under-active” a common state of "inhibited prime movers." Although both of these scenarios are legitimate possibilities, they are also relatively rare; only accounting for a small portion of muscles in each of the predictive models of dysfunction. Using these rationales in abundance can only lead to ineloquent analyses, like the table above. Further, this leads to fairly crude practice, as a muscle appearing on both sides of the table may be a rationale to use both mobility and activation techniques on the same muscle. In my humble opinion, a table with so many muscles on "both sides," should be an indication that further thought should be given to the joint actions that represent the movement impairment noted.

Third, the table above does not allow for a detailed analysis of changes in muscle activity (tone). Initially, it is possible to reason that short muscles are over-active, citing that over-activity may be a reason for the adaptively shortened position, or for creating the noted excessive motion, and the inverse can be said of long muscles, stating that under-activity allows for muscles to be "pulled" into a lengthened position, and reduces their ability to eccentrically decelerate the dysfunctional motion. However, this simple categorization of short muscles as over-active, and long muscles as under-active does not explain "synergistic dominance," "prime mover inhibition," "pattern overload," and other maladaptive changes in muscle activity and recruitment.

The fourth issue with the model above is the omission of several joints. For example, a sign commonly noted in those exhibiting LED is “

.” The amount of "turn-out" observed in those with significant dysfunction (often 20-45°) cannot be achieved via subtalar abduction alone (15). As this often occurs during sitting, sit-to-stand transfers, and at the bottom squat, lunge, and bilateral jumping patterns, the turn-out cannot be credited to femoral external rotation either - femoral external rotation at the bottom of a squat would bring the feet together as if to assume the "lotus position" in yoga. 

, must be a function of tibial external rotation at the 

 (optimal available range for tibial external rotation = 45°(15)). This implies that the 

 should be included in a model of LED. As many of the rotators of the 

 mechanics may also be affected. We can make further biomechanical inferences regarding the relationship between the 

, considering that tibia external rotation is relative to femoral internal rotation. Later in this article, research will be discussed that demonstrates a relationship between 

 motion. Even the proximal and distal tibiofibular joints play a role, but as their motions are best described as slide and roll their inclusion in the LED model will be limited to arthrokinematic analysis.

Fifth, this model misses analysis that would infer the use of effective techniques intended to alleviate arthrokinematic dysfunction (mobilizations, manipulations, muscle energy techniques) and fascial dysfunction (pin and stretch, myofascial release, IASTM, etc). That is to say that the traditional model of "Pronation Dysfunction" does not consider arthrokinematics or fascial dyskinesis. If the body is an adaptable, integrated system then all tissue systems should be accounted for. Further, an integrated model of practice would include a rationale for the effectiveness of all evidence-supported techniques. Additional analysis and consideration of research regarding arthrokinematics and fascia will be needed if the LED model is to be a comprehensive model of lower extremity impairments.

Last, despite considerable research correlating pain and altered movement, the analysis above does not attempt to identify related diagnoses and pathologies.

Summary of Issues with the "Traditional" Model:

Pronation is a term that is used differently by different professions to describe various aspects of foot/ankle motion, and therefore, is poorly defined.

Several joints that are likely related to these impairments have been omitted; this is discussed in detail under an "Evidence-based Osteokinematic Analysis"

Muscles appear on both long and short sides of the table without a clear reason (muscles cannot be long and short at the same time).

Description of this model does not allow for analysis of muscle activity of all muscles crossing the ankle.

Fascial structures have been excluded from this analysis.

Arthorkinematic dysfunction has been excluded from this analysis.

No attempt is made in this analysis to identify diagnoses and pathologies related to LED.

Considering the Traditional Model of Lower Extremity Dysfunction

As mentioned above, the LED model could be defined by those impairments that appear in the body of research, as well as the synonyms used and/or similar impairments. This includes:

 (inadequate forward translation of the knee, i.e. tibia on foot dorsiflexion)

 (a.k.a. functional pes planus, pronation, eversion, calcaneus valgus, positive navicular drop test, etc.)

 (a.k.a. functional knee valgus, medial knee displacement, hip adduction, etc.)

 (a.k.a. turn-out, heel flare, heel whip, etc.)

 (excessive hip flexion, forward trunk position, tibia/torso angle)

Note: in this case, "functional" is used as an adjective describing altered motion that is not caused by structural change or congenital abnormalities.

Signs of Lower Extremity Dysfunction

: Decreased dorsiflexion may be the most common "driver" of compensation in the lower extremity. Several studies have noted a link between decreased dorsiflexion, alterations in lower extremity alignment, and altered muscle recruitment during functional tasks (18-20, 23-28). That is, a decrease in dorsiflexion has been identified in studies investigating 

. Further, many of these studies correlated these patterns with commonly noted ankle and knee pathologies (medial knee pain, Achilles tendonitis, etc.). Although not commonly correlated with dysfunction unto itself, one study did show that 

self-administered release and stretching of the calf complex

 was effective for the treatment of plantar heel pain, with dorsiflexion being an outcome measure (43).

 (Functional Pes Planus) - Increased pronation has been associated with injuries ranging from medial tibial stress syndrome (shin splints) to tibialis posterior tendonitis, Achilles bursitis or tendinitis, patellofemoral disorders, iliotibial friction syndrome, and lower extremity stress fractures (29 - 39, 44, 48). It has been suggested that a combination of excessive pronation and internal tibial rotation (at the ankle) is a better predictor of the development of overuse injuries than either alone, especially of the 

 motions infers a connection with this sign/impairment 

 discussed below. In a study by Trimble et al., the sign was assessed with a lower extremity 

 and was found to be a more reliable indicator of tibial translation than recurvatum or thigh/foot angle (20). Further, excessive eversion has been linked to excessive 

 – Only two studies have correlated feet turn-out with dysfunction. In a study by Winslow et al., 

 pain (46), and in a study by Andrew et al., feet turn out was correlated with a functional varus and linked to 

 osteoarthritis (47). Another potential example of this dysfunction may be "medial heel whip"; a sign studied in runners in which the heel tracks medial during early swing. In a study by Souza et al., a medial heel whip of greater than 5° was noted in approximately 27% of individuals (45), although further study is needed to correlate this sign with pathology and recruitment. It is worth noting that tibial external rotation may also be a component of “

” (functional valgus), as femoral internal rotation can be viewed as relative tibial external rotation during closed chain activities.

 (functional valgus) – Research has correlated a functional valgus with a decrease in 

 activity, sacroiliac joint dysfunction, excessive 

 internal rotation and adduction, a loss of dorsiflexion, and excessive pronation (16, 23, 44 - 60). Studies have also correlated this sign of dysfunction with increased risk of 

 cruciate ligament (ACL) injury and patellofemoral pain (ACL) (16, 50, 51). Several studies have also noted the effectiveness of specific exercise interventions for correcting this dysfunction (23, 56 - 57).

 – Two studies have shown a relationship between dorsiflexion restriction and excessive hip flexion during squatting (in conjunction with other changes in lower extremity kinematics) (55, 61). Two additional studies have demonstrated a decrease in 

 strength and activity related to ankle dysfunction (42, 62), which may partially explain the inability to maintain an upright 

Based on this research, external rotation of the tibia, hip flexion, and hip internal rotation should be added to the analysis of LED (again, muscles in red appear on both sides of the graph).

Summary of Issues with the "Evidence-Based Osteokinematic Analysis"

To create a detailed model of practice, a model that will help to refine exercise selection, further analysis is required to determine the relative changes in activity of all muscles included in LED. In this "level of analysis," an attempt is made to aggregate all relevant research on all muscles included in the model.

Length Tension Relationship

Short/Over-active

Long/Over-active (Over-active Synergists)

Long/Under-active

Muscle Dysfunction: Summary of Research

Evidence-Based Muscular Approach

Our understanding of fascia has benefited from an exponential increase in research over the past two decades. This includes research on its traditional functions as a passive medium that supports, protects, and encapsulates tissues (145), as well as being a tissue that stores energy for explosive activity via elastic deformation (146, 147). However, the most interesting new research implicates fascia as a medium of communication. Levangin hypothesized that this may occur via electrical, cellular, and/or mechanical signals (148). Histological studies have shown this tissue to be densely innervated by free nerve endings, as well as by Pacinian corpuscles and Ruffini endings (145, 146). These findings have inspired my analogy of fascia as "nature's keyboard." Stecco et al. has demonstrated that deep fascia is arranged in layers that may slide over one another (147). This finding is likely most responsible for inspiring various fascia-specific interventions, and most often referred to when describing fascia's role in "interrupting" optimal motion. Carvalhais et al. demonstrated that tension may be transmitted through fascial sheaths to investing musculature, and Vleeming et al. has demonstrated the ability of fascia to transmit the force of multiple muscles to aid in joint stabilization (149, 173, 175).

Research also suggests the existence of myofibroblasts within the fascia, which may give the fascia the ability to contract. This ability is limited when compared to skeletal muscle tissue; however, the force generated was found to be significant enough to alter mechanics (in the lumbar spine) (150). It should also be noted that contraction in this study was very slow and in response to the antihistaminic substance, mepyramine (similar to smooth muscle), and these cells do not respond to electricity, tension, or sympathetic hormones. Although these findings do not lend themselves to practical application, they do inspire more hypotheses regarding the importance and function of this previously ignored tissue.

Fascia as a Passive Tissue (Traditional Functions):

Fascia as an Active Medium of Communication

Innervated with free nerve endings, Pacinian corpuscles, and Ruffini endings

Arranged in layers that slide over one another

May transmit tension between invested musculature

May transmit the force of multiple muscles to aid in joint stabilization

Fibroblasts may play a role in increasing tension in the fascia and altering mechanics.

A growing body of research has started to investigate the effect movement impairment has on fascial tissue, and what role fascial dysfunction may play in contributing to movement impairment. This statement by Schleip is a great example of the beginnings of an integration of these two fields, "tonic muscles contain more perimysium and are therefore stiffer than phasic muscles" (151). The terms, tonic and phasic refer to a categorization of muscles based on their roles in maintaining posture and/or contributing to postural dysfunction (1).

Fascia does seem to follow a predictable set of responses to excessive stress. This includes thickening, histochemical changes, decrease in tensile strength (increased risk of rupture), and the addition of disordered collagen fibers (156, 157, 161 - 165, 169 - 172). These consistent changes may have important implications for how these tissues should be addressed.

Crural Fascia

Plantar Fascia and Achilles Tendon

TFL and Iliotibial band (connecting fascia)

Iliotibial Band

Sacrotuberous Ligament

Fascial Dysfunction: Summary of Research

Introduction of Fascia into a Predictive Model of Movement Impairment

Research leading to the development of hypotheses on myofascial synergies (also known as slings or subsystems, and similar to the serape effect) (5, 178, 179) has influenced how the Brookbush Institute selects core exercises and integrated movement patterns. It is our belief that research on these myofascial synergies is an important step toward investigating recruitment patterns as they occur; as opposed to looking at isolated structures without the perspective of their role in an integrated system. You may note that many of the references in this section are the same as those cited in previous sections. The redundancy is not purposeful but is evidence that the research in the muscular and fascial sections are related to the additional studies demonstrating synergistic behavior or force transfer between fascial sheaths that have been added to this section. As each subsystem is discussed in detail in separate articles, only a brief summary of relevant research, function, and hypothesized behavior relative to LED is given below.

Posterior oblique subsystem (notice latissimus dorsi, thoracolumbar fascia and gluteus maximus)

Posterior Oblique Subsystem

Anterior Oblique Subsystem

Deep Longitudinal Subsystem

Myofascial Subsystems: Summary of Research

Myofascial Synergy a.k.a. Subsystems

As mentioned earlier, if various approaches are effective for different reasons (as implied by the varied intents), then an integrated approach may have the potential to improve outcomes by addition of the various benefits. Based on this premise, a weakness of the previous analyses (Traditional, Osteokinematic, Muscular, Fascial and Myofascial Synergies) is a failure to consider the effectiveness of well-established joint-based approaches. For example, osteopathic medicine, chiropractic, Cyriax/Maitland, Mulligan, Paris, etc.. Although measuring the small amounts of motion associated with arthrokinematics poses a considerable challenge for researchers, the body of research is growing. Further, several studies have noted a change in muscular activity as a result of joint mobilizations (213, 229, 241, 242). It is the assertion of the Brookbush Institute, that evidence of joint mobilizations affecting muscle activity supports the premise of a holistic system of human movement and an integrated approach, as mentioned at the beginning of this article. In this “level of analysis,” an attempt is made to aggregate all 

 research on altered arthrokinematics associated with impairments of the lower extremity (LED).

Arthrokinematic Dysfunction

Most of the research investigating the motion of the talus relates to an acute 

 instability (CAI). It is our hypothesis that these conditions are related to LED, as LED either predisposes an individual to such injuries or may be the result of these injuries. Further, an inability to glide the talus posteriorly is most often correlated with a 

 was used to define LED in the "Evidence-based Osteokinematic Analysis." In a study by Denegar et al., laxity was significantly greater at the talocrural and subtalar joints in participants with a recent history (6 months) of an 

 sprain; however, anterior to posterior glide of the talus on the tibia (AP glide) remained restricted, even when dorsiflexion returned to normal (195). A very similar relationship was found in those with CAI; side to side motion was not markedly different, posterior to anterior motion of the talus on the tibia was hypermobile; however, stiffness was noted when an attempt was made to AP glide (196). Adding a potential reason for these findings, in a study by Wikstrom et al., a correlation was made between CAI and an anteriorly shifted talus (anterior positional fault) (197). Based on the findings by Wikstrom et al. and the 

 associated with LED, it seems plausible that AP stiffness may be the result of adaptive shortening of posterior structures of the ankle ("squeezing the talus" anteriorly). This would be congruent with the "Evidence-based Muscular Analysis", as the 

 are prone to over-activity and adaptive shortening, and evidence of a loss of extensibility in posterior fascial structures (posterior capsule, Achilles tendon, crural fascia, etc.) seems plausible based on the findings in the Evidence-based Fascial Analysis. In practice, AP glide mobilizations have been correlated with improvements in dorsiflexion (198, 200, 202 - 204, 207), a reduction in pain (even in acute cases) (198, 199, 204), improvements in postural control (200, 202), fewer PT visits post-injury (198), and improvements in landing mechanics (201). Oddly, traction mobilization of the ankle does not appear to be beneficial for this same group (205, 206).

 malleolus on the tibia (distal tibiofibular joint) or hypermobility

 appears to have two common dysfunctional patterns (212). One scenario results in an anterior position fault (inadequate posterior glide) of the fibula on the tibia and hypomobility (197, 209); the other results in hypermobility and a posterior position fault when the foot is dorsiflexed (208, 210-212). This assessment of the research seems to be supported by the Whitman et al. clinical prediction rule, as distal 

 stiffness was one of 5 signs indicating a higher likelihood of positive outcomes using joint manipulation post ankle sprain (214). Clinically, the release of the 

 has also proven helpful in increasing distal 

Lower Extremity Dysfunction (LED): Predictive Model of Lower Extremity Movement Impairment

Related Courses:

Course Description: Lower Extremity Dysfunction (LED)

Introduction

Summary of Model
5 Sub Sections

Considering the Traditional Model of Lower Extremity Dysfunction

Signs of Lower Extremity Dysfunction

Osteokinematic Dysfunction
1 Sub Section

Evidence-Based Muscular Approach
4 Sub Sections

Introduction of Fascia into a Predictive Model of Movement Impairment
5 Sub Sections

Myofascial Synergy a.k.a. Subsystems
4 Sub Sections

Arthrokinematic Dysfunction

Ankle
3 Sub Sections

Symptoms, Injuries and Diagnoses Associated with Lower Extremity Dysfunction LED

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Lower Extremity Dysfunction (LED): Predictive Model of Lower Extremity Movement Impairment

Related Courses:

Course Description: Lower Extremity Dysfunction (LED)

Introduction

Summary of Model5 Sub Sections

Considering the Traditional Model of Lower Extremity Dysfunction

Signs of Lower Extremity Dysfunction

Osteokinematic Dysfunction1 Sub Section

Evidence-Based Muscular Approach4 Sub Sections

Introduction of Fascia into a Predictive Model of Movement Impairment5 Sub Sections

Myofascial Synergy a.k.a. Subsystems4 Sub Sections

Arthrokinematic Dysfunction

Ankle3 Sub Sections

Symptoms, Injuries and Diagnoses Associated with Lower Extremity Dysfunction LED

Thank You

Bibliography

Related Courses:

Comments

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Summary of Model
5 Sub Sections

Osteokinematic Dysfunction
1 Sub Section

Evidence-Based Muscular Approach
4 Sub Sections

Introduction of Fascia into a Predictive Model of Movement Impairment
5 Sub Sections

Myofascial Synergy a.k.a. Subsystems
4 Sub Sections

Ankle
3 Sub Sections