Research Article: Antagonist muscle activity during reactive balance responses is elevated in Parkinson’s disease and in balance impairment

Date Published: January 25, 2019

Publisher: Public Library of Science

Author(s): Kimberly C. Lang, Madeleine E. Hackney, Lena H. Ting, J. Lucas McKay, Erika Franzén.

http://doi.org/10.1371/journal.pone.0211137

Abstract

Abnormal antagonist leg muscle activity could indicate increased muscle co-contraction and clarify mechanisms of balance impairments in Parkinson’s disease (PD). Prior studies in carefully selected patients showed PD patients demonstrate earlier, longer, and larger antagonist muscle activation during reactive balance responses to perturbations.

Here, we tested whether antagonist leg muscle activity was abnormal in a group of PD patients who were not selected for phenotype and most of whom had volunteered for exercise-based rehabilitation.

We compared antagonist activation during reactive balance responses to multidirectional support-surface translation perturbations in 31 patients with mild-moderate PD (age 68±9; H&Y 1–3; UPDRS-III 32±10) and 13 matched individuals (age 65±9). We quantified modulation of muscle activity (i.e., the ability to activate and inhibit muscles appropriately according to the perturbation direction) using modulation indices (MI) derived from minimum and maximum EMG activation levels observed across perturbation directions.

Antagonist leg muscle activity was abnormal in unselected PD patients compared to controls. Linear mixed models identified significant associations between impaired modulation and PD (P<0.05) and PD severity (P<0.01); models assessing the entire sample without referencing PD status identified associations with balance ability (P<0.05), but not age (P = 0.10). Antagonist activity is increased during reactive balance responses in PD patients who are not selected on phenotype and are candidates for exercise-based rehabilitation. This activity may be a mechanism of balance impairment in PD and a potential rehabilitation target or outcome measure.

Partial Text

Abnormal antagonist muscle activity can cause joint stiffening by concurrently activating paired agonist and antagonist muscles (“co-contraction” or “co-activation”) [1–4], which may contribute to balance impairment in people with Parkinson’s disease (PD). Prior studies in PD patients carefully selected for postural difficulties and minimal tremor [5, 6] demonstrate earlier, longer, and larger antagonist muscle activation during reactive balance responses to perturbations of the support surface compared to controls [5–8]. Evaluation of antagonist muscle activation during balance could therefore potentially inform improved rehabilitative outcome measures (e.g., [9]). However, it is unclear whether antagonist muscle activity during reactive balance responses is abnormal in individuals with PD who are not selected by phenotype and are candidates for exercise-based rehabilitation. These individuals are often earlier in the disease course and may have milder symptoms than patients included in research studies without a rehabilitative component.

The main result of this study was that leg muscle activity during reactive balance was abnormal in a group of mild-moderate PD patients who were unselected for phenotype. We found that lower muscle modulation across perturbation directions–an estimate of an impaired ability to appropriately inhibit muscles according to the biomechanical requirements of the balance task– was predicted by the presence of PD and by PD severity, and that, importantly, these findings were common across the TD, PIGD, and indeterminate phenotypes. Overall, the current results are consistent with the findings of previous studies in PD patients [5, 7], many of which were conducted before standardized methods of calculating and reporting PD phenotypes based on UPDRS items were in common use, which supports the generalizability of earlier results. Taken together, these results provide additional evidence that antagonist muscle activation could be a useful rehabilitative target.

 

Source:

http://doi.org/10.1371/journal.pone.0211137

 

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