Relationships between coefficients of impairments at lower limb muscles in chronic spastic paresis–Could the muscle disease impact on the neurological disease?

Abstract

At the onset of hemiparesis, muscle tissue is normal and spastic overactivity is nil. Later, motor function becomes gradually hindered by: spastic myopathy (part of soft tissue contracture) and co-contraction, in addition to paresis. Relationships between these remain unclear. This retrospective study explores correlations between muscle shortening on one hand, and, spastic co-contraction and agonist paresis on the other hand. Eighty participants with chronic hemiparesis (29 W, 51 (± 13) years (mean (± SD)), time since lesion, 6.4 (± 3.2) years)) were assessed through the Five Step Assessment, at least three months after any botulinum toxin injection, in six key lower limb antagonists: soleus (SO), gastrocnemius (GN), gluteus maximus (GM), hamstrings (HS), vastus (VA), rectus femoris (RF). Coefficients of impairment were calculated as: coefficient of shortening (C SH = (X N − X V1 )/X N ; X N , normally expected amplitude; X V1 , angle of arrest upon slow stretch), coefficient of weakness (C W = (X V1 − X A )/X V1 ; X A , maximal active range of motion). For each muscle and for the mean of the six muscles, bivariate correlations between C SH and C W were explored, using Pearson's coefficients. The mean C SH are as follows: C SH-SO , 0.15 ± 0.05; C SH-GN , 0.17 ± 0.04; C SH-GM , 0.14 ± 0.08; C SH-HS , 0.06 ± 0.05; C SH-VA , 0.09 ± 0.05; C SH-RF , 0.13 ± 0.07. C W strongly correlated with C SH across the six muscles ( r = 0.30, P = 0.006). This correlation was also found individually for GN ( r = 0.43, P < 0.0001), GM ( r = 0.22, P = 0.04) and HS ( r = 0.21, P = 0.052). While causality is not explored in this study, one may speculate that spastic myopathy (assessed through coefficient of shortening) may play a role in neurologic impairments, potentially by chronic modifications of afferent volleys to the spinal cord.