Human Spinal Motor Control.

Human studies in the past three decades have provided us with an emerging understanding of how cortical and spinal networks collaborate to ensure the vast repertoire of human behaviors. Humans have direct cortical connections to spinal motoneurons, which bypass spinal interneurons and exert a direct (willful) muscle control with the aid of a context-dependent integration of somatosensory and visual information at cortical level. However, spinal networks also play an important role. Sensory feedback through spinal circuitries is integrated with central motor commands and contributes importantly to the muscle activity underlying voluntary movements. Regulation of spinal interneurons is used to switch between motor states such as locomotion (reciprocal innervation) and stance (coactivation pattern). Cortical regulation of presynaptic inhibition of sensory afferents may focus the central motor command by opening or closing sensory feedback pathways. In the future, human studies of spinal motor control, in close collaboration with animal studies on the molecular biology of the spinal cord, will continue to document the neural basis for human behavior.

Accurate Monitoring of 24-h Real-World Movement Behavior in People with Cerebral Palsy Is Possible Using Multiple Wearable Sensors and Deep Learning.

Monitoring and quantifying movement behavior is crucial for improving the health of individuals with cerebral palsy (CP). We have modeled and trained an image-based Convolutional Neural Network (CNN) to recognize specific movement classifiers relevant to individuals with CP. This study evaluates CNN's performance and determines the feasibility of 24-h recordings. Seven sensors provided accelerometer and gyroscope data from 14 typically developed adults during videotaped physical activity. The performance of the CNN was assessed against test data and human video annotation. For feasibility testing, one typically developed adult and one adult with CP wore sensors for 24 h. The CNN demonstrated exceptional performance against test data, with a mean accuracy of 99.7%. Its general true positives (TP) and true negatives (TN) were 1.00. Against human annotators, performance was high, with mean accuracy at 83.4%, TP 0.84, and TN 0.83. Twenty-four-hour recordings were successful without data loss or adverse events. Participants wore sensors for the full wear time, and the data output were credible. We conclude that monitoring real-world movement behavior in individuals with CP is possible with multiple wearable sensors and CNN. This is of great value for identifying functional decline and informing new interventions, leading to improved outcomes.

Contribution of sensory feedback to soleus muscle activity during voluntary contraction in humans.

Sensory feedback through spinal interneurons contributes to plantar flexor muscle activity during walking, but it is unknown whether this is also the case during nonlocomotor movements. Here, we explored the effect of temporary reduction of sensory feedback to ankle plantar flexors during voluntary contraction in sitting subjects. Thirteen healthy adults (mean age 32 yr) were seated with the right leg attached to a foot plate which could be moved in dorsi- or plantarflexion direction by a computer-controlled motor. EMG was recorded from the tibialis anterior (TA) and soleus (Sol) muscles. During static plantar flexion, while the plantar flexors were slowly stretched, a sudden plantar flexion caused a decline in Sol EMG at the same latency as the stretch reflex. This decline in EMG activity was still observed when transmission from dorsiflexors was blocked. It disappeared when transmission from ankle plantar flexors was also blocked. The same quick plantarflexion failed to produce a decline in EMG activity at the latency of the stretch reflex in the absence of slow stretch of the plantar flexors. Instead, a decline in EMG activity was observed 15-20 ms later. This decline disappeared following block of transmission from antagonists, suggesting that reciprocal inhibition was involved. These findings show that unload of ankle plantar flexors does not cause a similar drop in Sol EMG during voluntary contraction as during walking. This implies that sensory feedback through spinal interneurons only contributes little to the neural drive to plantar flexor muscles during human voluntary contraction in sitting subjects.NEW & NOTEWORTHY Sensory feedback through spinal reflex pathways makes only a minor contribution to neural drive to muscles during voluntary ankle plantar flexion. This differs distinctly from observations during walking and suggests that the neural drive to ankle plantar flexors during voluntary contraction do not rely on sensory feedback through similar spinal interneuronal networks as during walking. In line with animal studies this suggests that the integration of sensory feedback in CNS is task specific.

The effect of cathodal transspinal direct current stimulation on tibialis anterior stretch reflex components in humans.

Spinal DC stimulation (tsDCS) shows promise as a technique for the facilitation of functional recovery of motor function following central nervous system (CNS) lesion. However, the network mechanisms that are responsible for the effects of tsDCS are still uncertain. Here, in a series of experiments, we tested the hypothesis that tsDCS increases the excitability of the long-latency stretch reflex, leading to increased excitability of corticospinal neurons in the primary motor cortex. Experiments were performed in 33 adult human subjects (mean age 28 ± 7 years/14 females). Subjects were seated in a reclining armchair with the right leg attached to a footplate, which could be quickly plantarflexed (100 deg/s; 6 deg amplitude) to induce stretch reflexes in the tibialis anterior (TA) muscle at short (45 ms) and longer latencies (90-95 ms). This setup also enabled measuring motor evoked potentials (MEPs) and cervicomedullary evoked potentials (cMEPs) from TA evoked by transcranial magnetic stimulation (TMS) and electrical stimulation at the cervical junction, respectively. Cathodal tsDCS at 2.5 and 4 mA was found to increase the long-latency reflex without any significant effect on the short-latency reflex. Furthermore, TA MEPs, but not cMEPs, were increased following tsDCS. We conclude that cathodal tsDCS over lumbar segments may facilitate proprioceptive transcortical reflexes in the TA muscle, and we suggest that the most likely explanation of this facilitation is an effect on ascending fibers in the dorsal columns.

Corticomuscular coherence is reduced in relation to dorsiflexion fatigability to the same extent in adults with cerebral palsy as in neurologically intact adults.

PURPOSE: Fatigue is frequent in adults with cerebral palsy (CP) and it is unclear whether this is due to altered corticospinal drive. We aimed to compare changes in corticospinal drive following sustained muscle contractions in adults with CP and neurologically intact (NI) adults. METHODS: Fourteen adults with CP [age 37.6 (10.1), seven females, GMFCS levels I-II] and ten NI adults [age 35.4 (10.3), 6 females] performed 1-min static dorsiflexion at 30% of maximal voluntary contraction (MVC) before and after a submaximal contraction at 60% MVC. Electroencephalography (EEG) and electromyography (EMG) from the anterior tibial muscle were analyzed to quantify the coupling, expressed by corticomuscular coherence (CMC). RESULTS: Adults with CP had lower MVCs but similar time to exhaustion during the relative load of the fatigability trial. Both groups exhibited fatigability-related changes in EMG median frequency and EMG amplitude. The CP group showed lower beta band (16-35 Hz) CMC before fatigability, but both groups decreased beta band CMC following fatigability. There was a linear correlation between decrease of beta band CMC and fatigability-related increase in EMG. CONCLUSION: Fatigability following static contraction until failure was related to decreased beta band CMC in both NI adults and adults with CP. Our findings indicate that compensatory mechanisms to fatigability are present in both groups, and that fatigability affects the corticospinal drive in the same way. We suggest that the perceived physical fatigue in CP is related to the high relative load of activities of daily living rather than any particular physiological mechanism.

Gene expressions in cerebral palsy subjects reveal structural and functional changes in the gastrocnemius muscle that are closely associated with passive muscle stiffness.

Cerebral palsy (CP) is a non-progressive motor disorder that affects posture and gait due to contracture development. The purpose of this study is to analyze a possible relation between muscle stiffness and gene expression levels in muscle tissue of children with CP. Next-generation sequencing (NGS) of gene transcripts was carried out in muscle biopsies from gastrocnemius muscle (n = 13 children with CP and n = 13 typical developed (TD) children). Passive stiffness of the ankle plantarflexors was measured. Structural changes of the basement membranes and the sarcomere length were measured. Twelve pre-defined gene target sub-categories of muscle function, structure and metabolism showed significant differences between muscle tissue of CP and TD children. Passive stiffness was significantly correlated to gene expression levels of HSPG2 (p = 0.02; R2 = 0.67), PRELP (p = 0.002; R2 = 0.84), RYR3 (p = 0.04; R2 = 0.66), C COL5A3 (p = 0.0007; R2 = 0.88), ASPH (p = 0.002; R2 = 0.82) and COL4A6 (p = 0.03; R2 = 0.97). Morphological differences in the basement membrane were observed between children with CP and TD children. The sarcomere length was significantly increased in children with CP when compared with TD (p = 0.04). These findings show that gene targets in the categories: calcium handling, basement membrane and collagens, were significantly correlated to passive muscle stiffness. A Reactome pathway analysis showed that pathways involved in DNA repair, ECM proteoglycans and ion homeostasis were amongst the most upregulated pathways in CP, while pathways involved in collagen fibril crosslinking, collagen fibril assembly and collagen turnover were amongst the most downregulated pathways when compared with TD children. These results underline that contracture formation and motor impairment in CP is an interplay between multiple factors.

Directed connectivity between primary and premotor areas underlying ankle force control in young and older adults.

The control of ankle muscle force is an integral component of walking and postural control. Aging impairs the ability to produce force steadily and accurately, which can compromise functional capacity and quality of life. Here, we hypothesized that reduced force control in older adults would be associated with altered cortico-cortical communication within a network comprising the primary motor area (M1), the premotor cortex (PMC), parietal, and prefrontal regions. We examined electroencephalographic (EEG) responses from fifteen younger (20-26 â€‹yr) and fifteen older (65-73 â€‹yr) participants during a unilateral dorsiflexion force-tracing task. Dynamic Causal Modelling (DCM) and Parametric Empirical Bayes (PEB) were used to investigate how directed connectivity between contralateral M1, PMC, parietal, and prefrontal regions was related to age group and precision in force production. DCM and PEB analyses revealed that the strength of connections between PMC and M1 were related to ankle force precision and differed by age group. For young adults, bidirectional PMC-M1 coupling was negatively related to task performance: stronger backward M1-PMC and forward PMC-M1 coupling was associated with worse force precision. The older group exhibited deviations from this pattern. For the PMC to M1 coupling, there were no age-group differences in coupling strength; however, within the older group, stronger coupling was associated with better performance. For the M1 to PMC coupling, older adults followed the same pattern as young adults - with stronger coupling accompanied by worse performance - but coupling strength was lower than in the young group. Our results suggest that bidirectional M1-PMC communication is related to precision in ankle force production and that this relationship changes with aging. We argue that the observed differences reflect compensatory reorganization that counteracts age-related sensorimotor declines and contributes to maintaining performance.

Immobilization leads to reduced stretch reflexes but increased central reflex gain in the rat.

Plastic adaptations are known to take place in muscles, tendons, joints, and the nervous system in response to changes in muscle activity. However, few studies have addressed how these plastic adaptations are related. Thus this study focuses on changes in the mechanical properties of the ankle plantarflexor muscle-tendon unit, stretch reflex activity, and spinal neuronal pathways in relation to cast immobilization. The left rat hindlimb from toes to hip was immobilized with a plaster cast for 1, 2, 4, or 8 wk followed by acute electrophysiological recordings to investigate muscle stiffness and stretch reflex torque. Moreover, additional acute experiments were performed after 4 wk of immobilization to investigate changes in the central gain of the stretch reflex. Monosynaptic reflexes (MSR) were recorded from the L4 and L5 ventral roots following stimulation of the corresponding dorsal roots. Rats developed reduced range of movement in the ankle joint 2 wk after immobilization. This was accompanied by significant increases in the stiffness of the muscle-tendon complex as well as an arthrosis at the ankle joint at 4 and 8 wk following immobilization. Stretch reflexes were significantly reduced at 4-8 wk following immobilization. This was associated with increased central gain of the stretch reflex. These data show that numerous interrelated plastic changes occur in muscles, connective tissue, and the central nervous system in response to changes in muscle use. The findings provide an understanding of coordinated adaptations in multiple tissues and have important implications for prevention and treatment of the negative consequences of immobilization following injuries of the nervous and musculoskeletal systems.NEW & NOTEWORTHY Immobilization leads to multiple simultaneous adaptive changes in muscle, connective tissue, and central nervous system.

Spastic movement disorder: should we forget hyperexcitable stretch reflexes and start talking about inappropriate prediction of sensory consequences of movement?

Spastic movement disorder is characterized by reduced ability to selectively activate muscles with significant co-activation of antagonist muscles. It has traditionally been thought that hyperexcitable stretch reflexes have a central role in the pathophysiology and the clinical manifestations of the disorder. Here we argue that the main functional challenges for persons with spastic movement disorder are related to contractures, paresis, weak muscles and inappropriate central motor commands, whereas hyperexcitable reflexes play no or only an insignificant functional role. Co-activation of antagonist muscles and stiff posture and gait may rather be adaptations that aim to ensure joint and postural stability due to insufficient muscle strength. Aberrant (involuntary) muscle activity is likely related to an inadequate prediction of the sensory consequences of movement and a resulting impairment of muscle coordination. We argue that improvement of functional muscle strength and muscle coordination following central motor lesions may be achieved by optimizing integration of somatosensory information into central feedforward motor programs, whereas anti-spastic therapy that aims to reduce reflex activity may be less efficient. This opens for novel investigations into new treatment strategies that may improve functional control of movement and prevent reduced joint mobility in people with brain lesions.

Maturation of feedforward toe walking motor program is impaired in children with cerebral palsy.

Voluntary toe walking in adults is characterized by feedforward control of ankle muscles in order to ensure optimal stability of the ankle joint at ground impact. Toe walking is frequently observed in children with cerebral palsy, but the mechanisms involved have not been clarified. Here, we investigated maturation of voluntary toe walking in typically-developing children and typically-developed adults and compared it to involuntary toe walking in children with cerebral palsy. Twenty-eight children with cerebral palsy (age 3-14 years), 24 typically-developing children (age 2-14 years) and 15 adults (mean age 30.7 years) participated in the study. EMG activity was measured from the tibialis anterior and soleus muscles together with knee and ankle joint position during treadmill walking. In typically-developed adults, low step-to-step variability of the drop of the heel after ground impact was correlated with low tibialis anterior and high soleus EMG with no significant coupling between the antagonist muscle EMGs. Typically-developing children showed a significant age-related decline in EMG amplitude reaching an adult level at 10-12 years of age. The youngest typically-developing children showed a broad peak EMG-EMG synchronization (>100 ms) associated with large 5-15 Hz coherence between antagonist muscle activities. EMG coherence declined with age and at the age of 10-12 years no correlation was observed similar to adults. This reduction in coherence was closely related to improved step-to-step stability of the ankle joint position. Children with cerebral palsy generally showed lower EMG levels than typically-developing children and larger step-to-step variability in ankle joint position. In contrast to typically-developing children, children with cerebral palsy showed no age-related decline in tibialis anterior EMG amplitude. Motor unit synchronization and 5-15 Hz coherence between antagonist EMGs was observed more frequently in children with cerebral palsy when compared to typically-developing children and in contrast to typically-developing participants there was no age-related decline. We conclude that typically-developing children develop mature feedforward control of ankle muscle activity as they age, such that at age 10-12 years there is little agonist-antagonist muscle co-contraction around the time of foot-ground contact during toe walking. Children with cerebral palsy, in contrast, continue to co-contract agonist and antagonist ankle muscles when toe walking. We speculate that children with cerebral palsy maintain a co-contraction activation pattern when toe walking due to weak muscles and insufficient motor and sensory signalling necessary for optimization of feedforward motor programs. These findings are important for understanding of the pathophysiology and treatment of toe walking.

The development of functional and directed corticomuscular connectivity during tonic ankle muscle contraction across childhood and adolescence.

In adults, oscillatory activity in the sensorimotor cortex is coherent with contralateral muscle activity at beta frequencies (15-35 Hz) during tonic contraction. This functional coupling reflects the involvement of the sensorimotor cortex, the corticospinal pathway, and likely also ascending sensory feedback in the task at hand. However, little is known about the developmental trajectory of task-related corticomuscular connectivity relating to the voluntary control of the ankle muscles. To address this, we recorded electroencephalography (EEG) from the vertex (Cz) and electromyography (EMG) from ankle muscles (proximal and distal anterior tibial, TA; soleus, SOL; gastrocnemius medialis, GM) in 33 participants aged 7-23 yr during tonic dorsi- and plantar flexion requiring precise maintenance of a submaximal torque level. Coherence was calculated for Cz-TA, Cz-SOL, TA-TA, and SOL-GM signal pairs. We found strong, positive associations between age and beta band coherence for Cz-TA, Cz-SOL, and TA-TA, suggesting that oscillatory corticomuscular connectivity is strengthened during childhood development and adolescence. Directionality analysis indicated that the primary interaction underlying this age-related increase was in the descending direction. In addition, performance during dorsi- and plantar flexion tasks was positively associated with age, indicating more precise control of the ankle joint in older participants. Performance was also positively associated with beta band coherence, suggesting that participants with greater coherence also exhibited greater precision. We propose that these results indicate an age-related increase in oscillatory corticospinal input to the ankle muscle motoneuron pools during childhood development and adolescence, with possible implications for maturation of precision force control. Within the theoretical framework of predictive coding, we suggest that our results may reflect an age-related increase in reliance on feedforward control as the developing nervous system becomes better at predicting the sensory consequences of movement. These findings may contribute to the development of novel intervention strategies targeting improved sensorimotor control in children and adolescents with central motor disorders.

Contribution of corticospinal drive to ankle plantar flexor muscle activation during gait in adults with cerebral palsy.

Impaired plantar flexor muscle activation during push-off in late stance contributes importantly to reduced gait ability in adults with cerebral palsy (CP). Here we used low-intensity transcranial magnetic stimulation (TMS) to suppress soleus EMG activity during push-off as an estimate of corticospinal drive in CP adults and neurologically intact (NI) adults. Ten CP adults (age 34 years, SD 14.6, GMFCS I-II) and ten NI adults (age 33 years, SD 9.8) walked on a treadmill at their preferred walking speed. TMS of the leg motor cortex was elicited just prior to push-off during gait at intensities below threshold for motor-evoked potentials. Soleus EMG from steps with and without TMS were averaged and compared. Control experiments were performed while standing and in NI adults during gait at slow speed. TMS induced a suppression at a latency of about 40 ms. This suppression was similar in the two populations when differences in control EMG and gait speed were taken into account (CP 18%, NI 16%). The threshold of the suppression was higher in CP adults. The findings suggest that corticospinal drive to ankle plantar flexors at push-off is comparable in CP and NI adults. The higher threshold of the suppression in CP adults may reflect downregulation of cortical inhibition to facilitate corticospinal drive. Interventions aiming to facilitate excitability in cortical networks may contribute to maintain or even improve efficient gait in CP adults.

Characterization of torque generating properties of ankle plantar flexor muscles in ambulant adults with cerebral palsy.

PURPOSE: Weakness of plantar flexor muscles is related to reduced push-off and forward propulsion during gait in persons with cerebral palsy (CP). It has not been clarified to what an extent altered muscle contractile properties contribute to this muscle weakness. Here, we investigated the torque generating capacity and muscle fascicle length in the triceps surae muscle throughout ankle range of motion (ROM) in adults with CP using maximal single muscle twitches elicited by electrical nerve stimulation and ultrasonography. METHODS: Fourteen adults with CP (age 36, SD 10.6, GMFCS I-III) and 17 neurological intact (NI) adults (age 36, SD 4.5) participated. Plantar flexor torque during supramaximal stimulation of the tibial nerve was recorded in a dynamometer at 8 ankle angles throughout ROM. Medial gastrocnemius (MG) fascicle length was tracked using ultrasonography. RESULTS: Adults with CP showed reduced plantar flexor torque and fascicle shortening during supramaximal stimulation throughout ROM. The largest torque generation was observed at the ankle joint position where the largest shortening of MG fascicles was observed in both groups. This was at a more plantarflexed position in the CP group. CONCLUSION: Reduced torque and fascicle shortening during supramaximal stimulation of the tibial nerve indicate impaired contractile properties of plantar flexor muscles in adults with CP. Maximal torque was observed at a more plantarflexed position in adults with CP indicating an altered torque-fascicle length/ankle angle relation. The findings suggest that gait rehabilitation in adults with CP may require special focus on improvement of muscle contractility.

Effects on Parental Stress of Early Home-Based CareToy Intervention in Low-Risk Preterm Infants.

Parenting a preterm infant is more challenging than a full-term one. Parent involvement in early intervention programs seems to have positive psychosocial effects on both the child and parent. CareToy is an innovative smart system that provides an intensive individualized home-based family-centred EI in preterm infants between 3 and 9 age-corrected months. A RCT study, preceded by a pilot study, has been recently carried out to evaluate the effects of CareToy intervention on neurodevelopmental outcomes with respect to Standard Care. This study aims at evaluating the effects of CareToy early intervention on parenting stress in preterm infants. Parents (mother and father) of a subgroup of infants enrolled in the RCT filled out a self-report questionnaire on parenting stress (Parenting Stress Index-Short Form (PSI-SF)) before (T0) and after (T1) the CareToy or Standard Care period (4 weeks), according to the allocation of their preterm infant. For twins, an individual questionnaire for each one was filled out. Results obtained from mothers and fathers were separately analysed with nonparametric tests. 44 mothers and 44 fathers of 44 infants (24 CareToy/20 Standard Care) filled out the PSI-SF at T0 and at T1. CareToy intervention was mainly managed by mothers. A significant (p < 0.05) reduction in Parental Distress subscale in the CareToy group versus Standard Care was found in the mothers. No differences were found among the fathers. CareToy training seems to be effective in reducing parental distress in mothers, who spent more time on CareToy intervention. These findings confirm the importance of parental involvement in early intervention programs. This trial is registered with Clinical Trial.gov NCT01990183.

Sequence variants in muscle tissue-related genes may determine the severity of muscle contractures in cerebral palsy.

Muscle contractures are a common complication to cerebral palsy (CP). The purpose of this study was to evaluate whether individuals with CP carry specific gene variants of important structural genes that might explain the severity of muscle contractures. Next-generation-sequencing (NGS) of 96 candidate genes associated with muscle structure and metabolism were analyzed in 43 individuals with CP (Gross Motor Function classification system [GMFCS] I, n=10; GMFCS II, n=14; GMFCS III, n=19) and four control participants. In silico analysis of the identified variants was performed. The variants were classified into four categories ranging from likely benign (VUS0) to highly likely functional effect (VUS3). All individuals with CP were classified and grouped according to their GMFCS level: Statistical comparisons were made between GMFCS groups. Kruskal-Wallis tests showed significantly more VUS2 variants in the genes COL4 (GMFCS I-III; 1, 1, 5, respectively [p < .04]), COL5 (GMFCS I-III; 1, 1, 5 [p < .04]), COL6 (GMFCS I-III; 0, 4, 7 [p < .003]), and COL9 (GMFCS I-III; 1, 1, 5 [p < .04]), in individuals with CP within GMFCS Level III when compared to the other GMFCS levels. Furthermore, significantly more VUS3 variants in COL6 (GMFCS I-III; 0, 5, 2 [p < .01]) and COL7 (GMFCS I-III; 0, 3, 0 [p < .04]) were identified in the GMFCS II level when compared to the other GMFCS levels. The present results highlight several candidate gene variants in different collagen types with likely functional effects in individuals with CP.

Feedforward neural control of toe walking in humans.

KEY POINTS: Activation of ankle muscles at ground contact during toe walking is unaltered when sensory feedback is blocked or the ground is suddenly dropped. Responses in the soleus muscle to transcranial magnetic stimulation, but not peripheral nerve stimulation, are facilitated at ground contact during toe walking. We argue that toe walking is supported by feedforward control at ground contact. ABSTRACT: Toe walking requires careful control of the ankle muscles in order to absorb the impact of ground contact and maintain a stable position of the joint. The present study aimed to clarify the peripheral and central neural mechanisms involved. Fifteen healthy adults walked on a treadmill (3.0 km h-1 ). Tibialis anterior (TA) and soleus (Sol) EMG, knee and ankle joint angles, and gastrocnemius-soleus muscle fascicle lengths were recorded. Peripheral and central contributions to the EMG activity were assessed by afferent blockade, H-reflex testing, transcranial magnetic brain stimulation (TMS) and sudden unloading of the planter flexor muscle-tendon complex. Sol EMG activity started prior to ground contact and remained high throughout stance. TA EMG activity, which is normally seen around ground contact during heel strike walking, was absent. Although stretch of the Achilles tendon-muscle complex was observed after ground contact, this was not associated with lengthening of the ankle plantar flexor muscle fascicles. Sol EMG around ground contact was not affected by ischaemic blockade of large-diameter sensory afferents, or the sudden removal of ground support shortly after toe contact. Soleus motor-evoked potentials elicited by TMS were facilitated immediately after ground contact, whereas Sol H-reflexes were not. These findings indicate that at the crucial time of ankle stabilization following ground contact, toe walking is governed by centrally mediated motor drive rather than sensory driven reflex mechanisms. These findings have implications for our understanding of the control of human gait during voluntary toe walking.

Characterization of corticospinal activation of finger motor neurons during precision and power grip in humans.

Direct and indirect corticospinal pathways to finger muscles may play a different role in control of the upper extremity. We used transcranial magnetic stimulation (TMS) and coherence analysis to characterize the corticospinal drive to the first dorsal interosseous (FDI) and abductor pollicis brevis (APB) when active during a precision and power grip task. In experiment 1, single motor units were recorded during precision grip and power grip in 20 adults (25.2 ± 7.1 years). Post-stimulus time histograms (PSTH) were obtained following TMS. In experiment 2, coherence and cross-correlation analysis of the FDI and APB surface EMG were used to investigate the temporal organization of corticospinal drive during precision grip and power grip in 15 adults (27.4 ± 8.1 years). We found no significant differences in PSTH peak onset (26.6 ± 1.9 vs. 26.7 ± 2.0 ms, p = 0.75), maximal peak (27.4 ± 1.9 vs. 27.4 ± 1.9 ms, p = 1.0) or peak duration (2.3 ± 1.1 vs. 2.3 ± 1.0 ms, p = 0.75) for the 11 recovered motor units during precision grip and power grip. Also, no significant difference in coherence or the width of the synchronization peaks during precision grip (7.2 ± 3.7 ms) and power grip (7.9 ± 3.1 ms) could be observed (p = 0.59). The short duration of peaks elicited in the PSTH of single motor units following TMS and central synchronization peaks of voluntarily activated motor units during precision and power grip suggests that the direct corticospinal pathway (the corticomotoneuronal system) is equally involved in the control of both tasks. The data do not support that indirect pathways would make a larger contribution to power grip.

Impaired muscle growth precedes development of increased stiffness of the triceps surae musculotendinous unit in children with cerebral palsy.

AIM: If increased muscle stiffness and contractures in children with cerebral palsy (CP) are related to impaired muscle growth, reduced muscle growth should precede or coincide with increased muscle stiffness during development. Here, we compared the volume of the medial gastrocnemius muscle and the passive (non-neural) stiffness of the triceps surae musculotendinous unit in typically developing children and children with CP from birth until 4 years of age. METHOD: Forty-one children with CP and 45 typically developing children were included. Freehand three-dimensional ultrasound was used to evaluate the volume of the medial gastrocnemius muscle. Biomechanical and electrophysiological measures were used to determine passive and reflex mediated stiffness of the triceps surae musculotendinous unit. RESULTS: Medial gastrocnemius muscle volume increased with the same rate in typically developing and children with CP until 12 months of age, when a significant smaller rate of growth was observed in children with CP. Passive stiffness of the triceps surae musculotendinous unit showed a linear increase with age in typically developing children. Children with CP older than 27 months showed a significant increase in passive stiffness. Reflex mediated stiffness was only pathologically increased in four children with CP. INTERPRETATION: The deviation of medial gastrocnemius muscle volume, earlier than musculotendinous unit stiffness, is consistent with the hypothesis. The data also point out that muscle atrophy and muscle stiffness already develops within the first 1 to 2 years. This emphasizes the necessity of early interventions to promote lower limb muscle growth in this population. WHAT THIS PAPER ADDS: 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.

Impaired Ability to Suppress Excitability of Antagonist Motoneurons at Onset of Dorsiflexion in Adults with Cerebral Palsy.

We recently showed that impaired gait function in adults with cerebral palsy (CP) is associated with reduced rate of force development in ankle dorsiflexors. Here, we explore potential mechanisms. We investigated the suppression of antagonist excitability, calculated as the amount of soleus H-reflex depression at the onset of ankle dorsiflexion compared to rest, in 24 adults with CP (34.3 years, range 18-57; GMFCS 1.95, range 1-3) and 15 healthy, age-matched controls. Furthermore, the central common drive to dorsiflexor motoneurons during a static contraction in the two groups was examined by coherence analyses. The H-reflex was significantly reduced by 37% at the onset of dorsiflexion compared to rest in healthy adults (P < 0.001) but unchanged in adults with CP (P = 0.91). Also, the adults with CP had significantly less coherence. These findings suggest that the ability to suppress antagonist motoneuronal excitability at movement onset is impaired and that the central common drive during static contractions is reduced in adults with CP.

Oscillatory Corticospinal Activity during Static Contraction of Ankle Muscles Is Reduced in Healthy Old versus Young Adults.

Aging is accompanied by impaired motor function, but age-related changes in neural networks responsible for generating movement are not well understood. We aimed to investigate the functional oscillatory coupling between activity in the sensorimotor cortex and ankle muscles during static contraction. Fifteen young (20-26 yr) and fifteen older (65-73 yr) subjects were instructed to match a target force by performing static ankle dorsi- or plantar flexion, while electroencephalographic (EEG) activity was recorded from the cortex and electromyographic (EMG) activity was recorded from dorsi- (proximal and distal anterior tibia) and plantar (soleus and medial gastrocnemius) flexor muscles. EEG-EMG and EMG-EMG beta band (15-35 Hz) coherence was analyzed as an index of corticospinal activity. Our results demonstrated that beta cortico-, intra-, and intermuscular coherence was reduced in old versus young subjects during static contractions. Old subjects demonstrated significantly greater error than young subjects while matching target forces, but force precision was not related to beta coherence. We interpret this as an age-related decrease in effective oscillatory corticospinal activity during steady-state motor output. Additionally, our data indicate a potential effect of alpha coherence and tremor on performance. These results may be instrumental in developing new interventions to strengthen sensorimotor control in elderly subjects.