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Equinus (EFD) and equinovarus foot deviation (EVFD) are the most frequent lower limb deformities in stroke survivors. The equinus component can be triggered by a combination of dorsiflexor deficits, plantar flexor overactivity, muscle stiffness, and contractures. The varus component is typically due to an imbalance between invertor and evertor muscle actions. An improvement in identifying its causes leads to a more targeted treatment. These deformities are typically assessed via a thorough clinical evaluation including the assessment of range of motions, force, spasticity, pain, and observational gait analysis. Diagnostic nerve blocks are also being increasingly used. An advantage of dynamic electromyography (dEMG) is the possibility of measuring muscle activity, overactivity or lack thereof, during specific movements, e.g., activity of both ankle plantar flexors and dorsiflexors during the swing phase of gait. Moreover, fine-wire electrodes can be used to measure the activity of deep muscles, e.g., the tibialis posterior. An impediment to systematic use of dEMG in the assessment of EFD and EVFD, as a complimentary tool to the clinical evaluation, is a lack of evidence of its usefulness. Unfortunately, there are few studies found in literature. In order to fill this void, we studied three pairs of patients suffering from chronic hemiparesis consequent to a stroke, with EFD or EVFD. At the initial evaluation they all displayed the same clinical traits, very similar walking patterns, and an overlapping gait kinematics. However, the patterns of muscle activity differed considerably. dEMG data acquired during walking provided information that was not available from the sole clinical assessment. The contribution of this information to the subsequent clinical and rehabilitation process was discusses along with the barriers that limit the use of dEMG as a routine tool in neurorehabilitation.

Equinus deformity of the foot is a common feature of hemiplegia, which impairs the gait pattern of patients. The aim of the present study was to explore the role of ankle-foot deformity in gait impairment. A hierarchical cluster analysis was used to classify the gait patterns of 49 chronic hemiplegic patients with equinus deformity of the foot, based on temporal-distance parameters and joint kinematic measures obtained by an innovative protocol for motion assessment in the sagittal, frontal, and transverse planes, synthesized by parametrical analysis. Cluster analysis identified five subgroups of patients with homogenous levels of dysfunction during gait. Specific joint kinematic abnormalities were found, according to the speed of progression in each cluster. Patients with faster walking were those with less ankle-foot complex impairment or with reduced range of motion of ankle-foot complex, that is with a stiff ankle-foot complex. Slow walking was typical of patients with ankle-foot complex instability (i.e., larger motion in all the planes), severe equinus and hip internal rotation pattern, and patients with hip external rotation pattern. Clustering of gait patterns in these patients is helpful for a better understanding of dysfunction during gait and delivering more targeted treatment.

Early management of spasticity may improve stroke outcome. Botulinum toxin type A (BoNT-A) is recommended treatment for post-stroke spasticity (PSS). However, it is usually administered in the chronic phase of stroke. Our aim was to determine whether the length of time between stroke onset and initial BoNT-A injection has an effect on outcomes after PSS treatment. This multicenter, longitudinal, cohort study included stroke patients (time since onset <12 months) with PSS who received BoNT-A for the first time according to routine practice. The main outcome was the modified Ashworth scale (MAS). Patients were evaluated before BoNT-A injection and then at 4, 12, and 24 weeks of follow-up. Eighty-three patients with PSS were enrolled. MAS showed a significant decrease in PSS at 4 and 12 weeks but not at 24 weeks after treatment. Among the patients with a time between stroke onset and BoNT-A injection >90 days, the MAS were higher at 4 and 12 weeks than at 24 weeks compared to those injected ≤90 days since stroke. Our findings suggest that BoNT-A treatment for PSS should be initiated within 3 months after stroke onset in order to obtain a greater reduction in muscle tone at 1 and 3 months afterwards.