Hypomobility and Stiffness
This article defines joint hypomobility and stiffness from a biomechanical perspective, exploring their relationship and the underlying factors contributing to restricted joint movement.
Biomechanical Definition of Hypomobility
Hypomobility is biomechanically defined as a pathological limitation or significant reduction in the physiological range of motion (ROM) of a joint, encompassing either active, passive, or both, when compared to established normative data adjusted for factors such as age, sex, and contralateral limb status. It represents a quantifiable decrease in the joint's osteokinematic capacity, signifying less motion available than is considered normal or functional.
The observed reduction in osteokinematic ROM characteristic of hypomobility arises from underlying biomechanical constraints. These constraints can stem from:
Restricted Arthrokinematics: Impairment of the normal roll, glide, and/or spin between the joint surfaces is a primary cause. If the necessary accessory motions cannot occur freely, the larger physiological movement will be blocked. For example, restricted posterior glide of the talus on the tibia will limit ankle dorsiflexion.
Tissue Limitations: Changes in the properties or length of tissues surrounding the joint can restrict movement. These include:
- Intra-articular Factors: Adhesions within the joint, incongruity of joint surfaces, presence of loose bodies, or degenerative changes that alter surface geometry.
- Periarticular Factors: Shortening, thickening, or adherence of the joint capsule (capsular pattern of restriction), shortening or scarring of ligaments, adaptive shortening or contracture of muscles crossing the joint, or restrictions within the surrounding fascia.
- Neurological Factors: Protective muscle guarding or spasm, often secondary to pain or acute injury, can actively limit motion, mimicking or contributing to hypomobility.
Hypomobility is thus the clinical outcome—the measurable decrease in ROM—while the underlying causes are the biomechanical factors restricting normal osteokinematic and arthrokinematic motion. It is distinguished from simple inflexibility, which may be within normal variation, by implying a pathological restriction that impairs function or has the potential to cause dysfunction. Assessment of the "end-feel" during PROM testing can provide valuable clues about the nature of the restriction (e.g., a hard capsular feel versus a bony block versus an empty feel due to pain).
It is also important to consider the joint within its functional kinetic chain. Hypomobility in one segment can impose altered mechanical demands on adjacent segments. For instance, restricted hip extension (hypomobility) may force the lumbar spine into excessive extension (compensatory hypermobility or altered stress) during the terminal stance phase of gait. This occurs because functional tasks often require a composite ROM achieved through contributions from multiple joints. If one joint fails to contribute its expected share due to hypomobility, other joints in the chain must compensate by moving more or bearing increased load to accomplish the task. Over time, this compensation can lead to overuse, pain, or the development of instability in those adjacent, initially healthy segments. Consequently, a comprehensive assessment of hypomobility should evaluate not only the restricted joint but also the mobility and function of related segments within the kinetic chain.
Biomechanical Definition of Joint Stiffness
Joint stiffness, in biomechanical terms, is the passive resistance encountered when a joint is displaced, either linearly or angularly. It is a measure of the force or torque required to produce a unit change in joint position (deformation or angle). Mathematically, it represents the instantaneous slope of the passive load-deformation (or torque-angle) curve for the joint complex at a specific point in the range of motion. A higher stiffness implies greater resistance to movement.
The Load-Deformation Curve: The relationship between the applied passive load (force or torque) and the resulting joint displacement (linear or angular) is typically represented by a non-linear curve. This curve reflects the collective mechanical properties of all tissues crossing or comprising the joint. Key regions include :
- Toe Region: An initial phase of low resistance where minimal force produces relatively large displacement. This corresponds biomechanically to the uncrimping or straightening of collagen fibers in ligaments and tendons and initial slack being taken up in the periarticular tissues. This region is analogous to the "Neutral Zone" described for spinal segments.
- Elastic/Linear Region: Following the toe region, the curve becomes steeper, indicating increased stiffness. In this phase, the collagen fibers and other connective tissues are being stretched elastically. The slope (k) in this region (k=ΔF/Δx or k=ΔT/Δθ) represents the primary stiffness of the tissues. This region corresponds to the "Elastic Zone".
- Plastic Region and Failure Point: If the load exceeds the tissue's elastic limit (yield point), permanent deformation occurs (plastic region). Further loading leads to microfailure and eventually macroscopic rupture (ultimate failure point).
Contributing Factors: The overall passive stiffness of a joint is a composite property derived from multiple sources :
- Intra-articular Structures: The inherent properties of articular cartilage (e.g., resistance to compression due to proteoglycans ), the viscosity of synovial fluid, and the geometry of the joint surfaces.
- Periarticular Passive Tissues: The primary contributors to passive stiffness are typically the connective tissues surrounding the joint, including the joint capsule, ligaments, fascia, and the passive elastic components within muscles (e.g., intramuscular connective tissue, titin filaments). The amount, arrangement, and cross-linking of collagen fibers within these tissues are critical determinants of their stiffness.
- Active/Neural Factors: While stiffness is primarily defined passively, the apparent stiffness of a joint during movement or testing can be significantly influenced by the level of muscle activation (co-contraction increases stiffness substantially) , reflex muscle activity , and resting muscle tone.
Joint stiffness is not a constant value but is dependent on the joint angle (stiffness typically increases towards the end ranges of motion) and the velocity of movement due to the viscoelastic nature of biological tissues. Viscoelasticity means tissues exhibit both elastic (spring-like) and viscous (fluid-like resistance) properties, causing resistance to increase with faster movement speeds (damping) and exhibiting phenomena like stress relaxation and creep.
It is important for clinicians to recognize the distinction between the strict biomechanical definition of passive stiffness and the common clinical usage of the term. While biomechanical stiffness refers specifically to the passive resistance to deformation represented by the slope of the load-deformation curve , a patient's complaint of "stiffness" may encompass a broader range of experiences. This subjective feeling might include true increased passive tissue resistance, but could also reflect pain upon initiating movement (start-up pain), increased effort required to move the limb (perhaps due to underlying weakness or altered motor control), or active muscle guarding adopted consciously or subconsciously to protect a painful or unstable joint. Therefore, clinical assessment requires careful interpretation to differentiate true passive biomechanical stiffness from these other potential contributors to the patient's symptoms.
Pathological changes within the joint's constituent tissues can directly alter the load-deformation characteristics and increase passive stiffness. For example, in conditions involving fibrosis, such as post-immobilization contracture or diseases like Duchenne Muscular Dystrophy where muscle tissue is replaced by less compliant fibrotic and adipose tissue , the material properties of the periarticular structures change. Similarly, aging is associated with increased non-enzymatic cross-linking of collagen fibers and potential thickening of the joint capsule. These molecular and structural alterations make the tissues inherently less compliant. Biomechanically, this manifests as a steeper slope on the load-deformation curve, particularly in the elastic region, signifying that a greater force is needed to achieve a given amount of tissue elongation or joint displacement. This directly translates to an increase in the passive biomechanical stiffness of the joint complex.
Relationship Between Increased Stiffness and Hypomobility
Increased passive joint stiffness is intrinsically linked to joint hypomobility; indeed, elevated stiffness is often the primary biomechanical factor causing the reduction in ROM. While stiffness describes the resistance to motion within the available range, and hypomobility describes the limitation of that range , they are causally related.
The mechanism connecting increased stiffness to hypomobility involves the load-deformation behavior of the joint complex. When the passive tissues resisting motion (e.g., capsule, ligaments, passive muscle elements) become pathologically stiffer, their load-deformation curve shifts. The slope of the curve, particularly in the elastic zone, becomes steeper. This means that as the joint moves towards its end range, the internal resistance forces increase more rapidly for each increment of motion compared to a normal joint. Consequently, the physiological limit of motion—the point where passive resistance becomes substantial enough to halt further movement—is reached at a smaller angular displacement. This results in a reduced overall passive (and often active) ROM, which is the definition of hypomobility. Pathological processes such as capsular fibrosis following injury or immobilization, ligamentous scarring and shortening, adaptive muscle shortening leading to contracture, or the formation of intra-articular adhesions all act to increase this passive resistance, thereby restricting the joint's ability to move through its full potential range.
Clinically, interventions aimed at treating hypomobility, such as stretching, joint mobilization, or manipulation, are fundamentally designed to reduce passive stiffness. These techniques apply controlled forces to the restricted tissues with the goal of inducing plastic deformation (in the case of prolonged stretching or high-grade mobilization) or restoring normal arthrokinematic glide (low-grade mobilization), effectively shifting the load-deformation curve to the right. This allows for greater joint displacement before significant resistance is encountered, thereby increasing the available ROM.
Furthermore, both stiffness and hypomobility can be direction-specific. A joint might exhibit normal physiological ROM and feel appropriately compliant when moved into flexion, but demonstrate significantly increased resistance (stiffness) and a reduced end-range (hypomobility) when moved into extension. This occurs because different periarticular structures limit motion in different directions. For example, the posterior capsule and hamstring muscles primarily restrict hip flexion, while the anterior capsule (iliofemoral ligament) and hip flexor muscles restrict hip extension. Pathological changes, such as an adhesion in the posterior capsule or a shortened iliopsoas muscle, can selectively increase stiffness and limit motion in one direction more than others. This highlights the necessity for clinicians to assess ROM and qualitatively evaluate resistance (end-feel) in all relevant planes of motion for a given joint to fully characterize its mobility status and identify the specific structures contributing to any observed hypomobility.
Summary
| Feature | Hypomobility | Stiffness | Hypermobility | Instability |
|---|---|---|---|---|
| Primary Biomechanical Domain | Osteokinematics | Tissue Property | Passive Osteokinematics | Arthrokinematic Control |
| Key Biomechanical Feature | Decreased ROM | Increased passive resistance to deformation | Increased passive ROM | Excessive/uncontrolled arthrokinematic translation/rotation under load |
| Typical Load-Deformation/NZ | Reduced total displacement; potentially smaller NZ, earlier/steeper EZ | Steeper slope (esp. in EZ) | Increased total displacement; potentially larger NZ, later/shallower EZ | Pathologically increased Neutral Zone (NZ) size relative to total ROM |
| Primary System(s) Implicated | Passive (tissue restriction); Arthrokinematics | Passive (tissue properties) | Passive (tissue laxity/compliance) | Passive, Active, and/or Neural Control System Failure |
| Common Clinical Complaint | Restricted movement, tightness, end-range pain | Feeling "tight," increased effort to move | Asymptomatic OR pain, fatigue, dislocations (if HSD) | Joint "giving way," feeling loose/unstable, apprehension, subluxations |
| Primary Assessment Method(s) | Goniometry (AROM/PROM), End-feel, Joint Play | Passive resistance during PROM, End-feel | Goniometry (PROM), Beighton Score | Specific Stress Tests (e.g., Drawer, Apprehension), Neuromuscular Assessment |
| Relationship to Other Terms | Often caused by increased Stiffness | A cause of Hypomobility | A risk factor for Instability, but distinct from it | Can occur with Hypo-, Normo-, or Hypermobility |
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