Joint Control

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This article is part of a series.

• Joint Biomechanics
• Hypomobility
• Hypermobility
• Joint Control

This article delves deeper into the biomechanical factors that determine joint stability and mobility, focusing on the load-deformation properties of tissues, the concepts of the neutral and elastic zones, and the critical role of the neuromuscular system in maintaining joint control, particularly in the context of hypermobility.

Load-Deformation Curve

Tendon stress-strain curve (typical)

Ligament stress-strain curve (typical)

Typical ranges of stress and strain are indicated on the x and y axes.

The passive mechanical behavior of a joint is largely dictated by the properties of its surrounding periarticular connective tissues, primarily ligaments and the joint capsule. Their response to tensile loading is classically described by a stress-strain or load-deformation curve. Understanding this curve is key to interpreting joint mobility and stability:

Tissue Load-Deformation Curve Features:

• Toe Region: At low loads, the wavy collagen fibers within the tissue straighten out ("uncrimp"). This region exhibits low stiffness (high compliance), meaning considerable deformation occurs with minimal force application. This initial slack allows for physiological joint play.
• Elastic Region: Once the collagen fibers are straightened, the tissue begins to stretch elastically. In this region, deformation is roughly proportional to the applied load (approximating Hooke's Law), and the tissue will return to its original length when the load is removed. The slope of the curve in this region defines the tissue's stiffness. This region represents the tissue's resistance to physiological loads.
• Yield Point and Plastic Region: Beyond the elastic limit (yield point), microscopic failure of collagen fibers begins, and the tissue undergoes permanent (plastic) deformation. It will not fully return to its original length upon unloading. Loading into this range causes microtrauma.
• Ultimate Failure Point: With continued loading, macroscopic tearing occurs, leading to complete rupture of the tissue.

Neutral and Elastic Zones

A typical load-deflection curve from experimental data of a flexion-extension experiment on a goat lumbar spine segment. The range of motion (ROM) is the total range of deformation upon maximal loading (+/- 2 Nm in this example). The neutral zone is the area with the least internal resistance against bending, thus the steepest slope of the load-displacement curve. NZ indicates the neutral zone. In this concept, the neutral zone stiffness is the inverse tangent to the curve at the intersection points with the y-axis (straight lines).

The Neutral Zone (NZ) and Elastic Zone (EZ): These concepts, developed primarily in the context of spinal biomechanics but applicable conceptually to other synovial joints, describe distinct regions of the joint's overall load-displacement behavior, reflecting the underlying tissue properties.

• Neutral Zone (NZ): Defined as the portion of the physiological range of motion around the joint's neutral (mid-range) position where movement occurs with minimal internal passive resistance. This high-compliance, low-stiffness zone corresponds biomechanically to the toe region of the load-deformation curves of the surrounding ligaments and capsule. Within the NZ, joint stability is not primarily provided by passive tissue tension but relies heavily on neuromuscular control (muscle activation and proprioceptive feedback) to maintain joint congruency and control intersegmental motion.
• Elastic Zone (EZ): Represents the portion of the ROM approaching the physiological limits (end-range). In this zone, the passive periarticular tissues become increasingly taut, providing significant internal resistance to further movement. This corresponds to the elastic region of the tissue load-deformation curves, where stiffness is substantially higher than in the NZ. The EZ provides the primary passive restraint against excessive motion at the end ranges.

Relationship to Mobility and Stability Concepts: The characteristics of the load-deformation curve and the resulting NZ/EZ directly inform our understanding of the different mobility states:

• Stiffness: Quantified by the slope of the load-deformation curve, particularly within the EZ. Increased stiffness (steeper slope) means more resistance to movement in the EZ.
• Hypomobility: Often associated with increased stiffness (steeper slope in the EZ) and potentially a reduced size of the NZ, leading to a smaller overall ROM. The transition from NZ to EZ occurs earlier in the range.
• Hypermobility: Characterized by increased overall ROM. Biomechanically, this may correspond to an enlarged NZ, a delayed transition into the EZ, and/or decreased stiffness (shallower slope) within the EZ, reflecting greater tissue compliance.
• Instability: Defined by Panjabi specifically as a pathological increase in the size of the NZ relative to the total ROM. This signifies that the joint exhibits excessive, poorly controlled motion within the low-resistance mid-range under physiological loads, indicating a failure of the stabilizing systems (passive, active, or neural) to adequately constrain movement within this zone.

The size of the Neutral Zone often serves as a more sensitive indicator of joint instability than the total Range of Motion, particularly in the early stages of degenerative processes or following minor ligamentous injury. Initial pathological changes might primarily affect the joint's behavior under low loads, increasing the laxity around the neutral position (enlarging the NZ) before significantly impacting the end-range constraints that determine total ROM. Measuring only the total ROM could therefore fail to detect this subtle increase in mid-range laxity, which is biomechanically indicative of reduced stability. Consequently, biomechanical assessments that quantify the NZ can provide valuable insights into the joint's functional stability and its ability to control movement during everyday activities, which frequently occur within or near this low-stiffness zone.

It is also important to acknowledge that biological tissues exhibit viscoelasticity, meaning their mechanical response depends on the rate and duration of loading. Properties like stiffness and the measured size of the NZ are influenced by testing speed; faster movements generally encounter greater viscous resistance, leading to higher apparent stiffness. Furthermore, tissues exhibit hysteresis, where the loading and unloading curves do not overlap, indicating energy dissipation. This time- and rate-dependency means that stiffness and NZ parameters obtained from quasi-static tests may not perfectly reflect the joint's behavior during dynamic functional activities. Different methodologies used to calculate the NZ from load-deflection data can yield varying results, partly due to these viscoelastic effects, highlighting the need for standardized reporting and careful interpretation of these parameters.

The Role of Neuromuscular Control (Active Subsystem) in Joint Stability

While passive tissues provide the structural framework and end-range constraints, the neuromuscular system (comprising the active subsystem of muscles/tendons and the neural control subsystem) plays a vital, dynamic role in maintaining joint stability, especially under physiological loads and within the low-stiffness Neutral Zone. Without active muscle support, structures like the lumbar spine are inherently unstable and would buckle under minimal loads.

The neuromuscular system contributes to stability through several mechanisms:

• Joint Compression: Muscle contraction generates forces that compress joint surfaces together, enhancing congruency and frictional stability.
• Dynamic Stiffness Regulation: Muscles actively modulate joint stiffness by varying their level of contraction and co-contraction. Increased muscle activation, particularly simultaneous activation of agonist and antagonist muscles (co-contraction), significantly increases the overall stiffness of the joint complex, providing resistance against unexpected perturbations.
• Active Restraint: Muscles act as dynamic "guy wires," actively generating forces to counteract translations and rotations throughout the range of motion, supplementing the passive restraints provided by ligaments.
• Feedback Control: Proprioceptive information from mechanoreceptors within the joint capsule, ligaments, muscles (spindles), and tendons (GTOs) provides continuous feedback to the central nervous system about joint position, movement, and load. This sensory input allows the neural control system to rapidly adjust muscle activation patterns via reflexes and voluntary commands to maintain stability and respond effectively to perturbations.

The role of neuromuscular control becomes particularly critical in individuals with joint hypermobility. The inherent increase in passive laxity (often reflected as a larger NZ and lower passive stiffness) means that these individuals rely more heavily on their active and neural control systems to maintain functional stability and prevent injury. Effective muscle strength, endurance, coordination, and proprioceptive acuity are essential to dynamically control the excessive motion potential. Some evidence suggests that individuals with hypermobility may develop enhanced neuromuscular control strategies, such as improved active joint position sense, potentially as a compensatory adaptation to their underlying laxity. However, deficits in neuromuscular control are also common in symptomatic hypermobile populations, contributing to functional instability.

Functional instability arises specifically from deficits within this neuromuscular control loop. Even if the passive structures are intact (or hypermobile), impairments in proprioception, delayed muscle reaction times, abnormal muscle activation patterns, or poor sensorimotor integration can lead to inadequate dynamic stabilization during activity. This results in the joint feeling unstable or giving way, despite potentially having normal or even excessive passive ROM.

Interestingly, neuromuscular compensation strategies in individuals with hypermobility or instability can sometimes lead to a clinical presentation that appears "stiff" during functional activities. To protect the joint or avoid painful ranges, individuals might adopt patterns of increased muscle co-contraction or guarding. This active stiffening increases dynamic joint stability but can limit the functional excursion of the joint during tasks like walking, creating an apparent reduction in dynamic ROM despite underlying passive hypermobility. This highlights a potential paradox where passive laxity can result in functional stiffness due to neuromuscular adaptation, emphasizing the need for clinicians to assess both passive ROM and dynamic movement control.

Furthermore, the stability of appendicular joints (e.g., shoulder, hip, knee) is influenced by the stability of the core or trunk. The core acts as a proximal foundation for limb movement. Deficits in neuromuscular control of the lumbar spine and pelvis can lead to altered force transmission along the kinetic chain and compensatory movement patterns in the extremities. This may increase the stress on distal joints or place them in biomechanically disadvantageous positions, potentially contributing to or exacerbating appendicular instability. Therefore, particularly in individuals with generalized hypermobility who rely heavily on active control systems, assessment and rehabilitation of core stability may be an essential component of managing distal joint instability symptoms.

Resources

Neuromuscular control of postural and core stability - zemkova 2022.pdf - 825 KB (f)