Key points• It is often assumed that automatic movements such as walking require little conscious attention and it has therefore been argued that these movements require little cortical control.• In humans, however, the gait function is often heavily impaired or completely lost following cortical lesions such as stroke.• In this study we investigated synchrony between cortical signals recorded with electroencephalography (EEG) and electromyographic signals (EMG activity) recorded from the tibialis anterior muscle (TA) during walking.• We found evidence of synchrony in the frequency domain (coherence) between the primary motor cortex and the TA muscle indicating a cortical involvement in human gait function.• This finding underpins the importance of restoration of the activity and connectivity between the motor cortex and the spinal cord in the recovery of gait function in patients with damage of the central nervous system.Abstract Indirect evidence that the motor cortex and the corticospinal tract contribute to the control of walking in human subjects has been provided in previous studies. In the present study we used coherence analysis of the coupling between EEG and EMG from active leg muscles during human walking to address if activity arising in the motor cortex contributes to the muscle activity during gait. Nine healthy human subjects walked on a treadmill at a speed of 3.5-4 km h −1 . Seven of the subjects in addition walked at a speed of 1 km h −1 . Significant coupling between EEG recordings over the leg motor area and EMG from the anterior tibial muscle was found in the frequency band 24-40 Hz prior to heel strike during the swing phase of walking. This signifies that rhythmic cortical activity in the 24-40 Hz frequency band is transmitted via the corticospinal tract to the active muscles during walking. These findings demonstrate that the motor cortex and corticospinal tract contribute directly to the muscle activity observed in steady-state treadmill walking.

Aim Lack of muscle growth relative to bone growth may be responsible for development of contractures in children with cerebral palsy (CP). Here, we used ultrasonography to compare growth of the medial gastrocnemius muscle in children with and without CP. Method Twenty‐six children with spastic CP (15 males, 11 females; mean age 35mo, range 8–65mo) and 101 typically developing children (47 males, 54 females; mean age 29mo, range 1–69mo) were included. Functional abilities of children with CP equalled levels I to III in the Gross Motor Function Classification System. Medial gastrocnemius muscle volume was constructed from serial, transverse, two‐dimensional ultrasonography images. Results In typically developing children, medial gastrocnemius volume increased linearly with age. Among children with CP, medial gastrocnemius volume increased less with age and deviated significantly from typically developing children at 15 months of age (p<0.05). Bone length increased with age without significant difference (p=0.49). Interpretation Muscle growth in children with CP initially follows that of typically developing children, but decreases at 15 months of age. This may be related to reduced physical activity and neural activation of the muscle. Interventions stimulating muscle growth in young children with CP may be important to prevent contractures.

Rehabilitation following spinal cord injury is likely to depend on recovery of corticospinal systems. Here we investigate whether transmission in the corticospinal tract may explain foot drop (inability to dorsiflex ankle) in persons with spinal cord lesion. The study was performed in 24 persons with incomplete spinal cord lesion (C1 to L1) and 15 healthy controls. Coherence in the 10- to 20-Hz frequency band between paired tibialis anterior muscle (TA) electromyographic recordings obtained in the swing phase of walking, which was taken as a measure of motor unit synchronization. It was significantly correlated with the degree of foot drop, as measured by toe elevation and ankle angle excursion in the first part of swing. Transcranial magnetic stimulation was used to elicit motor-evoked potentials (MEPs) in the TA. The amplitude of the MEPs at rest and their latency during contraction were correlated to the degree of foot drop. Spinal cord injured participants who exhibited a large foot drop had little or no MEP at rest in the TA muscle and had little or no coherence in the same muscle during walking. Gait speed was correlated to foot drop, and was the lowest in participants with no MEP at rest. The data confirm that transmission in the corticospinal tract is of importance for lifting the foot during the swing phase of human gait.

AIM Clinical determination of spasticity is confounded by the difficulty in distinguishing reflex from passive contributions to muscle stiffness. There is, therefore, a risk that children with cerebral palsy (CP) receive antispasticity treatment unnecessarily. To investigate this, we aimed to determine the contribution of reflex mechanisms to changes in the passive elastic properties of muscles and tendons in children with CP.METHOD Biomechanical and electrophysiological measures were used to determine the relative contribution of reflex and passive mechanisms to ankle muscle stiffness in 35 children with spastic CP (21 males, 14 females; mean age 9y, SD 3y 4mo; range 3-15y) and 28 control children without CP (19 males, nine females; mean age 8y 11mo, SD 2y 10mo; range 3-15y). Twenty-seven children were diagnosed as having spastic hemiplegia, six with spastic diplegia, and two with spastic tetraplegia. According to the Gross Motor Function Classification System, 31 children were classified in level I, two in level II, and two in level III.RESULTS Only seven children with spastic CP showed reflex stiffness outside the range of the control children. In contrast, 20 children with spastic CP showed abnormal passive muscle stiffness (p<0.001). No correlation between increased reflex or increased passive muscle stiffness and age was observed within the age range studied.

Medial gastrocnemius muscle growth is reduced in children with cerebral palsy (CP) around 12 months after birth. Triceps surae musculotendinous unit stiffness is increased in children with CP around 27 months after birth. Reflex excitability is rarely increased in children with CP. Reduced muscle growth may be involved in the pathophysiology of contractures.