Abstract

BackgroundNet agonist muscle strength is in part determined by the degree of antagonist co-activation. The level of co-activation might vary in different neurological disorders causing weakness or might vary with agonist strength.AimThis study investigated whether antagonist co-activation changed a) with the degree of muscle weakness and b) with the nature of the neurological lesion causing weakness.MethodsMeasures of isometric quadriceps and hamstrings strength were obtained. Antagonist (hamstring) co-activation during knee extension was calculated as a ratio of hamstrings over quadriceps activity both during an isometric and during a functional sit to stand (STS) task (using kinematics) in groups of patients with extrapyramidal (n = 15), upper motor neuron (UMN) (n = 12), lower motor neuron (LMN) with (n = 18) or without (n = 12) sensory loss, primary muscle or neuromuscular junction disorder (n = 17) and in healthy matched controls (n = 32). Independent t-tests or Mann Witney U tests were used to compare between the groups. Correlations between variables were also investigated.ResultsIn healthy subjects mean (SD) co-activation of hamstrings during isometric knee extension was 11.8 (6.2)% and during STS was 20.5 (12.9)%. In patients, co-activation ranged from 7 to 17% during isometric knee extension and 15 to 25% during STS. Only the extrapyramidal group had lower co-activation levels than healthy matched controls (p < 0.05). Agonist isometric muscle strength and co-activation correlated only in muscle disease (r = -0.6, p < 0.05) and during STS in UMN disorders (r = -0.7, p < 0.5).ConclusionIt is concluded that antagonist co-activation does not systematically vary with the site of neurological pathology when compared to healthy matched controls or, in most patient groups, with strength. The lower co-activation levels found in the extrapyramidal group require confirmation and further investigation. Co-activation may be relevant to individuals with muscle weakness. Within patient serial studies in the presence of changing muscle strength may help to understand these relationships more clearly.

Highlights

  • Net agonist muscle strength is in part determined by the degree of antagonist coactivation

  • It is concluded that antagonist co-activation does not systematically vary with the site of neurological pathology when compared to healthy matched controls or, in most patient groups, with strength

  • The lower co-activation levels found in the extrapyramidal group require confirmation and further investigation

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Summary

Introduction

Net agonist muscle strength is in part determined by the degree of antagonist coactivation. Most neurology based co-activation studies have been undertaken in stroke patients or children with "cerebral palsy" where hypoxic ischaemic pathology relatively non selectively involves multiple CNS pathways and is associated with marked increases in muscle tone [13]. Such CNS involvement may include pyramidal, parapyramidal and extrapyramidal, cortical, subcortical and cerebellar structures as well as sensory and association pathways. It was of interest to investigate patient groups with weakness due to different pathologies to see whether more selective patho-physiological causes of weakness were associated with differing levels of co-activation It was unclear from the literature whether the level of co-activation systematically altered with the degree of weakness

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