Lower extremity antagonist muscle response following standing perturbation in subjects with cerebrovascular disease.

The onset, amplitude, and relative timing of opposing muscle groups during forward and backward body sway were investigated in standing subjects with hemiplegia and a normal control group. The agonist was the first muscle stretched by platform perturbation and the antagonist was the opposing muscle passively shortened by the movement stimulus. Tibialis anterior (T), quadriceps (Q), gastrocnemius (G) and hamstrings (H) were simultaneously monitored bilaterally for burst activity. During rotational (toe up/down) and horizontal perturbations in normals, two distinct muscle responses were observed--an initial long-latency response (LLR) in the agonist and a subsequent response in the antagonist muscle group. Hemiplegics showed early activation of the antagonist response (AR) with respect to the initial LLR and frequent coactivation of synergists (T-Q or G-H). Although the AR was tightly coupled to the initial LLR in both hemiplegic lower limbs, initiation of the distal LLR-AR sequence was significantly delayed in the paretic extremity by 25-40 ms. In addition, the distal AR amplitude was suppressed in the paretic limb. The number of AR defaults in hemiplegics for all perturbation modes was significantly greater than normal. Therefore, unilateral cerebrovascular disease may reduce the occurrence of antagonist muscle activation and alter the latency, amplitude and phasing of passively shortened antagonist muscles.