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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.

The reliability of a computerized analysis system (CAS) for determining muscle burst onset was compared with the subjective assessments of three trained examiners. A sample of 154 randomly selected, full-wave rectified and filtered electromyographic recordings was evaluated using a test-retest paradigm. Percentages of agreement, Pearson product-moment correlations, analyses of variance (ANOVAs), and intraclass correlation coefficients (ICCs) were used to measure the reliability. The between-rater agreement, which included the computerized EMG assessments, was only 23%. Within-rater agreement and Pearson correlation coefficients were perfect for CAS. The trained examiners' within-rater assessments averaged only 51% agreement, but test-retest correlations were high (r = .78 - r = .82). All ICCs were statistically significant, ranged from .46 to .60, and tended to be higher when the CAS onset determinations were deleted from the analysis. The ANOVAs revealed that trained examiners were more consistent among each other than when their assessments were compared with CAS assessments of EMG recordings. This finding, however, may be facility-specific in that any generalization to other examiners was limited. In contrast to trained examiners, the CAS was free of variations in judgment, ensured perfect reproducibility of trial assessments, and was highly useful for analyzing multi-channel EMG recordings. Although the CAS ensures perfect reliability, validity determinations require visual inspection of trial data.

The symmetry and adaptability of long latency stretch responses was studied in a group of 4 adult hemiplegics and 5 normals of similar age. Subjects stood on a moveable platform which directly rotated the ankles unexpectedly during a series of horizontal anterioposterior (AP) translations. When the platform was rotated toes-up, long latency discharge of gastrocnemius and hamstring muscles enhanced loss of balance by pulling the body backwards. Toes-down platform rotation elicited a reflex response from tibialis anterior and quadriceps which inappropriately pulled the body forward. Attenuation of these long latency responses was necessary to minimize functional destabilization. Normal and stroke subjects demonstrated appropriate suppression of long latency responses, but the magnitude of attenuation was not uniform in hemiplegics. Adaptation was decreased in the proximal synergists compared to normal. Latency of muscle activation in the paretic limb was prolonged, and a preference for initial non-paretic limb activation was evident. Both lower extremities in hemiplegics showed a disruption of timing between distal and proximal synergists. These results suggest that stroke victims retain or recover the ability to modulate stretch reflex activity for balance. Temporal and spatial response asymmetries surface as critical factors underlying disequilibrium associated with localized cerebrovascular lesion.