Reflex and non-reflex elements of hypertonia in triceps surae muscles following acquired brain injury: implications for rehabilitation

Following adult onset acquired brain injury, the triceps surae muscles tend to become shortened and exhibit increased resistance to passive lengthening; a phenomenon that has been termed 'hypertonia'. Spasticity (velocity dependent tonic reflex hyper-excitability) has traditionally been considered a major component of hypertonia. In addition, unmodulated descending excitatory influences on the alpha motorneurone pool may result in inappropriate or excessive muscle activity (dystonia). Non-reflex changes, secondary to the brain injury, and as a consequence of subsequent immobility, also take place in the passive and active elements of the muscle. These non-reflex changes affect the stiffness and extensibility of the musculo-tendinous unit. Atrophy of muscle fibres combines with collagen proliferation to produce increased muscle stiffness. This may be compounded by increased actin-myosin cross-bridge linkages, which are thought to be associated with reduced rates of cross-bridge detachment. Prolonged immobilization in a shortened position results in a loss of sarcomeres in series. Arthrogenic changes associated with disuse include remodelling of dense connective tissue and intra-articular adhesions.

Decreased muscle extensibility may be exacerbated by muscle overactivity. Consideration of all of the potential factors contributing to hypertonia of the triceps surae muscle will assist clinicians to identify appropriate intervention strategies, which may facilitate better treatment outcomes.