Clinical Predictors of Ambulation Speed in Chronic Hemiparesis: A Structural Equation Approach

To elucidate the respective roles of key pathophysiological features, that is, spastic myopathy, spasticity, and descending command impairment, in impeding ambulation speed (AS) in chronic hemiparesis to help guide the treatment.

Retrospective study.

Neurorehabilitation unit.

Subjects with chronic hemiparesis.

A single clinician used the Five Step Assessment to measure maximal 10-m barefoot AS and 3 clinical estimates of the pathophysiological features above on 6 key lower limb antagonist muscles (gluteus maximus, hamstrings, vasti, rectus femoris, soleus, and gastrocnemius): (1) angle of arrest on slow and strong passive movement, estimating maximal clinical extensibility (X_V1); (2) angle of catch during fast movement estimating spasticity (X_V3); (3) angle of match between maximal agonist effort and passive and active antagonist resistances (maximal amplitude of active motion against the tested antagonist; X_A).

Relationships between AS and the various technical parameters were modeled using structural equations.

Data from 70 patients with chronic hemiparesis were collected (23 women [32.9%], age 51±16y, time since lesion 8±7y, main cause, stroke [81.4%]). Determinants of AS were better identified when classified through pathophysiological features (all muscles pooled together) rather than through individual muscles (all features pooled). Across muscles, the clinical parameter most strongly associated with AS was X_A (ß_std=0.69; P<.001), which itself depended on X_V1 (ß_std=0.68; P<.001). When considering individual muscles, AS is most strongly associated with X_A against vastus (ß_std-XA-VA=0.80; P<.001) and rectus femoris (ß_std-XA-RF=0.76; P<.001).

In chronic hemiparesis, AS is primarily associated with passive and active knee extensor antagonist resistances.