This paper examines the physiological changes in spastic muscles contributing to spasticity and muscle stiffness, focusing on the underlying mechanisms and their clinical implications. Spasticity, which is prevalent in neurological conditions such as multiple sclerosis, cerebral palsy, spinal cord injury, stroke, and traumatic brain injury, is characterized by disordered sensorimotor control and often results in increased muscle stiffness and resistance to movement. Recent developments in the understanding of spasticity suggest the importance of architectural changes in muscles that may contribute to increased passive resistance, potentiate reflex mechanisms, and progression to fibrosis, with hyaluronan (HA), a glycosaminoglycan, playing a pivotal in modulating the properties of the muscle extracellular matrix (ECM). The hyaluronan hypothesis of muscle stiffness postulates that the accumulation and biophysical alteration of HA in the ECM of muscle increases its viscosity, resulting in increased passive mechanical resistance. This is turn mayincrease muscle sensitivity to stretch, potentiating spasticity, and lead to cellular differentiation of myofibroblasts to fibroblasts ultimately leading to fibrosis and contracture. A deeper understanding of HA's role in ECM dynamics offers promising avenues for novel treatments aimed at mitigating stiffness and preventing long-term disability in patients with spasticity.