Fig. 2

Pathophysiology of arthrofibrosis secondary to neuromuscular disorders. Central nervous system (CNS) disruptions can damage the Upper or Lower motor neuron. UMN lesions lack cortical inhibitory signaling but increase excitability in the gamma and alpha motor neurons (distally at the spinal cord), causing spastic paresis. Overactivated spastic muscles lose balance with their corresponding antagonist muscles and suffer from “pulling” the entire limb into a deformed posture. With time, the contracted (shortened) muscle undergoes length adaptation decreasing the number of sarcomeres continuously until it becomes a fixed muscle contraction. On the other hand, lesions in the spinal cord or peripheral axons represent LMN lesions. These lesions cause denervation, atrophy, and flaccid paralysis, leading to muscle contractures. Both UMN/LMN lesions may present neurogenic growth disturbances if the contractured muscle grows at a different rate than the bone (aggravating the contraction and leading to bone deformities). As the muscle shortens in patients with NMD, the joint becomes immobilized in an abnormal position. With time, pathophysiological changes in the muscle-tendon unit and the periarticular soft tissue occur, including 1) replacement of sarcomeres with fibrofatty connective tissue that will reach the joint space, 2) loss of elasticity and extensibility as the connective tissue forms more cross-bridges with collagen and 3) a higher ratio of connective to contractile tissue (as the connective tissue loss is less rapidly). All this together will ultimately cause arthrofibrosis with a decrease in ROM both histologically and clinically. [References] [2, 5, 8,9,10,11,12]