Do Muscle Changes Contribute to the Neurological Disorder in Spastic Paresis?

Maud Pradines,Blaise Bignami,Emilie Hutin,Nicolas Bayle,Christina Marciniak,David Burke,Jordan Vielotte,Jean-Michel Gracies,Mouna Ghédira

doi:10.3389/fneur.2022.817229

Abstract

BackgroundAt the onset of stroke-induced hemiparesis, muscle tissue is normal and motoneurones are not overactive. Muscle contracture and motoneuronal overactivity then develop. Motor command impairments are classically attributed to the neurological lesion, but the role played by muscle changes has not been investigated.MethodsInteraction between muscle and command disorders was explored using quantified clinical methodology—the Five Step Assessment. Six key muscles of each of the lower and upper limbs in adults with chronic poststroke hemiparesis were examined by a single investigator, measuring the angle of arrest with slow muscle stretch (XV1) and the maximal active range of motion against the resistance of the tested muscle (XA). The coefficient of shortening CSH = (XN-XV1)/XN (XN, normally expected amplitude) and of weakness CW = (XV1-XA)/XV1) were calculated to estimate the muscle and command disorders, respectively. Composite CSH (CCSH) and CW (CCW) were then derived for each limb by averaging the six corresponding coefficients. For the shortened muscles of each limb (mean CSH > 0.10), linear regressions explored the relationships between coefficients of shortening and weakness below and above their median coefficient of shortening.ResultsA total of 80 persons with chronic hemiparesis with complete lower limb assessments [27 women, mean age 47 (SD 17), time since lesion 8.8 (7.2) years], and 32 with upper limb assessments [18 women, age 32 (15), time since lesion 6.4 (9.3) years] were identified. The composite coefficient of shortening was greater in the lower than in the upper limb (0.12 ± 0.04 vs. 0.08 ± 0.04; p = 0.0002, while the composite coefficient of weakness was greater in the upper limb (0.28 ± 0.12 vs. 0.15 ± 0.06, lower limb; p < 0.0001). In the lower limb shortened muscles, the coefficient of weakness correlated with the composite coefficient of shortening above the 0.15 median CSH (R = 0.43, p = 0.004) but not below (R = 0.14, p = 0.40).ConclusionIn chronic hemiparesis, muscle shortening affects the lower limb particularly, and, beyond a threshold of severity, may alter descending commands. The latter might occur through chronically increased intramuscular tension, and thereby increased muscle afferent firing and activity-dependent synaptic sensitization at the spinal level.

Highlights

In spastic paresis, muscle changes coexist with neurologic abnormalities [1, 2] and the two have been suggested to potentiate each other [3–5]
We retrospectively reviewed the charts of subjects with chronic hemiparesis that had been consecutively evaluated using at least steps 1, 2, and 4 of the Five Step Assessment [30] in the lower and/or the upper limb, by a single clinician (JMG) between January 2014 and December 2019 (Figure 1)
Of 110 consecutive patients with adult-onset chronic hemiparesis in whom the lower limb was evaluated during the study period, 80 patients met the criteria for inclusion

Summary

Introduction

Muscle changes coexist with neurologic abnormalities [1, 2] and the two have been suggested to potentiate each other [3–5]. Muscle mass is reduced and muscle extensibility decreases, in parallel with sarcomere loss [10–12]; in addition, collagen tissue is modified and deposits around muscle fibers with fascial thickening [13–16] These muscle changes can be demonstrated through biomechanical and clinical measurements; they gradually worsen if hypo-mobilization is not addressed [16–21]. Among the various types of muscle overactivity in spastic paresis, spastic cocontraction has been defined as a misdirection of the supraspinal drive that abnormally recruits antagonist motor units during agonist command, independent of any phasic stretch [5, 26, 27]. This form of overactivity directly impedes and may sometimes reverse the desired voluntary movement [26]. Motor command impairments are classically attributed to the neurological lesion, but the role played by muscle changes has not been investigated

Methods

Results

Discussion

Conclusion