Chronic low back pain as a control failure state: a predictive-rhythm model of motor control impairment and functional rigidity with functional system constraint modulation.

Motor dysfunction in chronic low back pain (CLBP) is commonly described at the output level-altered movement patterns, reduced variability, and maladaptive behaviors. Yet such output-level descriptions leave recurring clinical questions unresolved: why altered patterns begin, why apparent correction often fails to generalize, why stress and physiological state modulate function, and why performance fluctuates despite stable structure. We hypothesize that a subset of CLBP presentations can be conceptualized as a persistent control failure state when stabilization-dominant regulation, reduced adaptive variability, impaired phase-transition dynamics, and constrained predictive updating become self-maintaining features of motor behavior. In this framework, stabilization does not mean trunk stability alone; it denotes a regulatory strategy that minimizes uncertainty by reducing variability, restricting phase transitions, and prioritizing predictability over adaptability. Functional rigidity is treated as the clinical output expression of this state, characterized by reduced rhythmic variability, autonomic inflexibility, and anticipatory co-contraction, with altered kinematics emerging as a downstream biomechanical expression rather than the primary explanatory level. Respiratory-autonomic dynamics are introduced not as a privileged cause of CLBP but as one clinically accessible example of a broader class of phase-transition interfaces through which constrained regulation can be observed, perturbed, and quantified during task transitions and repetition. Functional System Constraint modulation (FSCm) is therefore not proposed as a universal CLBP theory or a proprietary intervention protocol. Rather, it is a constraint-level validation architecture that aligns three interacting mechanistic features-restricted phase transitions, reduced adaptive variability, and constrained predictive updating-with measurable recovery targets: restoration of phase-transition capacity, re-expansion of adaptive variability, re-enablement of predictive updating, and re-coupling of interacting rhythms. The model yields falsifiable temporal predictions: phase-transition and autonomic changes should precede or co-occur with reductions in stabilization-based motor output, while variability and repetitive-task performance may partially dissociate from pain intensity. By positioning FSCm as a complementary framework that integrates predictive coding, motor control impairment, nociplastic pain, and behavioral models, this hypothesis specifies target populations, boundary conditions, operational markers, and temporal-order falsification criteria for mechanistic CLBP research.