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We tested the hypothesis that the ipsilateral corticospinal system, like the contralateral corticospinal system, controls the threshold muscle length at which wrist muscles and the stretch reflex begin to act during holding tasks. Transcranial magnetic stimulation was applied over the right primary motor cortex in 21 healthy subjects holding a smooth or coarse block between the hands. Regardless of the lifting force, motor evoked potentials in right wrist flexors were larger for the smooth block. This result was explained based on experimental evidence that motor actions are controlled by shifting spatial stretch reflex thresholds. Thus, the ipsilateral corticospinal system is involved in threshold position control by modulating facilitatory influences of hand skin afferents on motoneurons of wrist muscles during bimanual object manipulation.

Galvanic vestibular stimulation (GVS) is used to assess vestibular system function, but vestibulospinal responses can exhibit variability depending on protocols or intensities used. Here, we measured head acceleration in healthy subjects to identify an objective motor threshold on which to base GVS intensity when assessing standing postural responses. Thirteen healthy right-handed subjects stood on a force platform, eyes closed, and head facing forward. An accelerometer was placed on the vertex to detect head acceleration, and electromyography activity of the right soleus was recorded. GVS (200 ms; current steps 0.5, from 1 mA to 4 mA) was applied in a binaural and bipolar configuration.

Background After a traumatic brain injury, disturbances in the attentional processes have a direct negative effect on functional recovery and on return to complex activities. To date, there is no good attention remediation treatment available. The primary objective of this review and pilot study is to provide an overview of the research evidence and to evaluate the feasibility of implementing a tDCS protocol to improve attention disorders in patients with mild complicated to severe subacute TBI, hospitalized in an inpatient rehabilitation facility. Our secondary objective is to extract preliminary data and observational information on participants’ response to treatment. Methods Participants were recruited from a consecutive series of patients admitted to the TBI unit of a subspecialized regional rehabilitation center. They received a 20-min tDCS stimulation 3 times a week for 3 weeks. A neuropsychological evaluation was performed before and after the intervention. We collected participants’ sociodemographic and clinical characteristics as well as information about satisfaction, tolerability, and adverse effects. Results One hundred sixty-four patients were admitted between September 2018 and January 2020. One hundred fifty-eight were excluded, and 6 patients with presumed attentional deficits were enrolled. None completed the protocol as intended. No major side effects occurred. Conclusion Non-invasive brain neurostimulation is promising to enhance attention deficits in patients with TBI. Implementation of a tDCS protocol to fulfill this purpose in an intensive inpatient rehabilitation center has its limitations. We made recommendations to facilitate the implementation of similar projects in the future. Trial registration ISRCTN, ISRCTN55243064. Registered 14 October 2020—retrospectively registered.

Individuals with incomplete spinal cord injury (iSCI) show altered postural reactions leading to increased risk of falls. To investigate neural correlates underlying this deficit, we assessed the modulation pattern of the Soleus H-reflex in iSCI individuals following unexpected perturbations of a base of support. Ten men with iSCI (AIS D) and 8 age-matched controls (CTRL) stood on a force-platform randomly tilted forward or backward. The center of pressure (CoP) excursion, 95% confidence ellipse area and electromyographic (EMG) activity of the Soleus (SOL) and Tibialis Anterior (TA) muscles were analyzed. SOL H-reflex amplitude was assessed by stimulating the tibial nerve prior to and at 100, 150 and 200 ms following perturbation onset. Although SOL and TA short-latency EMG responses were comparable in both groups, long-latency EMG responses occurred later in the iSCI group for both directions: during backward tilt, a decrease in H-reflex amplitude was observed at all stimulus timings post-tilt in CTRL, but only at 200 ms in iSCI. The decrease in H-reflex amplitude was smaller in iSCI participants. During forward tilt, an increase in H-reflex amplitude was observed at 150 and 200 ms in the CTRL group, but no increase was observed in the iSCI group. Decreased and delayed SOL H-reflex amplitude modulation in the iSCI group accompanied impaired balance control as assessed clinically with the Berg Balance Scale and biomechanically through CoP displacement. Overall, delayed and reduced spinal reflex processing may contribute to impaired balance control in people with iSCI.

Purpose To determine the effectiveness of a single 10-min postural repositioning session on the maximum phonation duration (MPD) of the vowel/a/in individuals with acquired dysarthria. Materials and methods A pre-post interventional design was implemented; five patients with dysarthria (PWDs) underwent a single 2-hour experimental session. MPD capacities were assessed before and immediately after a 10-min postural repositioning intervention by a physical and occupational therapist. Five age- and sex-matched individuals without dysarthria were recruited as controls. The main outcome measure was the MPD of the vowel/a/at conversational and louder voice levels, with a speech-and-language therapist standing 1 and 6 m away, respectively. Secondary outcome measures were thoracic expansion, manometry, electromyographic recordings of axial muscles and perceived effort. Results In PWDs, postural repositioning improved the MPD during the/a/-1-m (80.3% increase) and/a/-6-m tasks (18% increase), increased thoracic expansion and manometric measurements, and reduced the perceived effort necessary to perform the tasks. A triphasic electromyographic pattern was observed during both/a/-1-m and/a/-6-m tasks in controls, but was absent in participants with severe dysarthria, even after postural repositioning. Nonetheless, postural repositioning enabled an earlier onset of EMG activity prior to voice production. Conclusions These data suggest the efficacy of postural repositioning in improving phonatory capacities essential for voice production in PWDs.

Proprioceptive cervicogenic dizziness (PCGD) is the most prevalent subcategory of cervicogenic dizziness. There is considerable confusion regarding this clinical syndrome’s differential diagnosis, evaluation, and treatment strategy. Our objectives were to conduct a systematic search to map out characteristics of the literature and of potential subpopulations of PCGD, and to classify accordingly the knowledge contained in the literature regarding interventions, outcomes and diagnosis. A Joanna Briggs Institute methodology-informed scoping review of the French, English, Spanish, Portuguese and Italian literature from January 2000 to June 2021 was undertaken on PsycInfo, Medline (Ovid), Embase (Ovid), All EBM Reviews (Ovid), CINAHL (Ebsco), Web of Science and Scopus databases. All pertinent randomized control trials, case studies, literature reviews, meta-analyses, and observational studies were retrieved. Evidence-charting methods were executed by two independent researchers at each stage of the scoping review. The search yielded 156 articles. Based on the potential etiology of the clinical syndrome, the analysis identified four main subpopulations of PCGD: chronic cervicalgia, traumatic, degenerative cervical disease, and occupational. The three most commonly occurring differential diagnosis categories are central causes, benign paroxysmal positional vertigo and otologic pathologies. The four most cited measures of change were the dizziness handicap inventory, visual analog scale for neck pain, cervical range of motion, and posturography. Across subpopulations, exercise therapy and manual therapy are the most commonly encountered interventions in the literature. PCGD patients have heterogeneous etiologies which can impact their care trajectory. Adapted care trajectories should be used for the different subpopulations by optimizing differential diagnosis, treatment, and evaluation of outcomes.

Study design Observational, cohort study. Objectives (1) Determine the feasibility and relevance of assessing corticospinal, sensory, and spinal pathways early after traumatic spinal cord injury (SCI) in a rehabilitation setting. (2) Validate whether electrophysiological and magnetic resonance imaging (MRI) measures taken early after SCI could identify preserved neural pathways, which could then guide therapy. Setting Intensive functional rehabilitation hospital (IFR). Methods Five individuals with traumatic SCI and eight controls were recruited. The lower extremity motor score (LEMS), electrical perceptual threshold (EPT) at the S2 dermatome, soleus (SOL) H-reflex, and motor evoked potentials (MEPs) in the tibialis anterior (TA) muscle were assessed during the stay in IFR and in the chronic stage (>6 months post-SCI). Control participants were only assessed once. Feasibility criteria included the absence of adverse events, adequate experimental session duration, and complete dataset gathering. The relationship between electrophysiological data collected in IFR and LEMS in the chronic phase was studied. The admission MRI was used to calculate the maximal spinal cord compression (MSCC). Results No adverse events occurred, but a complete dataset could not be collected for all subjects due to set-up configuration limitations and time constraints. EPT measured at IFR correlated with LEMS in the chronic phases (r = −0.67), whereas SOL H/M ratio, H latency, MEPs and MSCC did not. Conclusions Adjustments are necessary to implement electrophysiological assessments in an IFR setting. Combining MRI and electrophysiological measures may lead to better assessment of neuronal deficits early after SCI.

Background Postural strategies are enabled by rapid muscle activation sequences to prevent a fall. Intralimb muscular couplings underlie these postural strategies are likely impaired after incomplete spinal cord injury (iSCI), leading to inappropriate postural reactions and increased fall risk; yet, the nature of these changes is unknown. Research question Identify changes occurring in intralimb coupling following a perturbation in individuals with iSCI. Methods Ten men with iSCI and eight age-matched controls (CTRL) stood on a force-platform that was randomly tilted forward or backward. Electromyographic (EMG) activity of the lower limb muscles was recorded, and coactivation or simultaneous facilitation/suppression between pairs of muscles was analyzed. Onset and duration of coupling latency, intralimb coupling delay, and amplitude ratios were measured in the distal (soleus [SOL]/tibialis anterior [TA]), proximal (biceps femoris [BF]/vastus lateralis [VL]), anterior (TA-VL), and posterior (SOL-BF) muscle couplings. Results In forward tilt, the main coupling was TA-SOL co-contraction for both groups, but the latency was longer and the duration shorter in SCI participants. In backward tilt, the TA-VL co-activation was the main coupling in CTRL (88 %), although it was also expressed by 60 % of SCI participant with a delayed latency. The facilitation/suppression of TA-SOL was the main coupling in SCI group (80 % vs 63 % in CTRL). Delayed coupling latencies were more pronounced in individuals with cervical iSCI and were correlated with the strength of lower limbs. Significance Similar muscular couplings are present in both groups but are delayed, which might contribute to postural reaction deficits in individuals with iSCI.

Unilateral arm movements require trunk stabilization through bilateral contraction of axial muscles. Interhemispheric interactions between primary motor cortices (M1) could enable such coordinated contractions, but these mechanisms are largely unknown. Using transcranial magnetic stimulation (TMS), we characterized interhemispheric interactions between M1 representations of the trunk-stabilizing muscles erector spinae at the first lumbar vertebra (ES L1) during a right isometric shoulder flexion. These interactions were compared with those of the anterior deltoid (AD), the main agonist in this task, and the first dorsal interosseous (FDI). TMS over the right M1 elicited ipsilateral silent periods (iSP) in all three muscles on the right side. In ES L1, but not in AD or FDI, ipsilateral motor evoked potential (iMEP) could precede the iSP or replace it. iMEP amplitude was not significantly different whether ES L1 was used to stabilize the trunk or was voluntarily contracted. TMS at the cervicomedullary junction showed that the size of cervicomedullary evoked potential was unchanged during the iSP but increased during iMEP, suggesting that the iSP, but not the iMEP, is due to intracortical mechanisms. Using a dual-coil paradigm with two coils over the left and right M1, interhemispheric inhibition could be evoked at interstimulus intervals of 6 ms in ES L1 and 8 ms in AD and FDI. Together, these results suggest that interhemispheric inhibition is dominant when axial muscles are involved in a stabilizing task. The ipsilateral facilitation could be evoked by ipsilateral or subcortical pathways and could be used depending on the role axial muscles play in the task. NEW & NOTEWORTHY The mechanisms involved in the bilateral coordination of axial muscles during unilateral arm movement are poorly understood. We thus investigated the nature of interhemispheric interactions in axial muscles during arm motor tasks in healthy subjects. By combining different methodologies, we showed that trunk muscles receive both inhibitory and facilitatory cortical outputs during activation of arm muscles. We propose that inhibition may be conveyed mainly through interhemispheric mechanisms and facilitation by subcortical mechanisms or ipsilateral pathways.

There are contralateral and less studied ipsilateral (i), indirect cortical descending projections to motoneurons (MNs). We compared ipsilateral cortical descending influences on MNs of wrist flexors by applying transcranial magnetic stimulation (TMS) over the right primary motor cortex at actively maintained flexion and extension wrist positions in uni- and bimanual tasks in right-handed participants (n = 23). The iTMS response includes a short latency (~ 25 ms) motor evoked potential (iMEP), a silent period (iSP) and a long latency (~ 60 ms) facilitation called rebound (iRB). We also investigated whether the interaction between the two hands while holding an object in a bimanual task involves ipsilateral cortical descending influences. In the unimanual task, iTMS responses in the right wrist flexors were unaffected by changes in wrist position. In the bimanual task with an object, iMEPs in the right wrist flexors were larger when the ipsilateral wrist was in flexion compared to extension. Without the object, only iRB were larger when the ipsilateral wrist was extended. Thus, ipsilateral cortical descending influences on MNs were modulated only in bimanual tasks and depended on how the two hands interacted. It is concluded that the left and right cortices cooperate in bimanual tasks involving holding an object with both hands, with possible involvement of oligo- and poly-synaptic, as well as transcallosal projections to MNs. The possible involvement of spinal and transcortical stretch and cutaneous reflexes in bimanual tasks when holding an object is discussed in the context of the well-established notion that indirect, referent control underlies motor actions.

When balance is compromised, postural strategies are induced to quickly recover from the perturbation. However, neuronal mechanisms underlying these strategies are not fully understood. Here, we assessed the amplitude of the soleus (SOL) H-reflex during forward and backward tilts of the support surface during standing (n = 15 healthy participants). Electrical stimulation of the tibial nerve was applied randomly before platform tilt (control) and 0, 25, 50, 75, 100 or 200 ms after tilt onset. During backward tilt, a significant decrease in H-reflex amplitude was observed at 75, 100 and 200 ms. The onset of the decreased H-reflex amplitude significantly preceded the onset of the SOL EMG decrease (latency: 144 ± 16 ms). During forward tilt, the amplitude of the H-reflex increased at 100 and 200 ms after tilt onset. The onset of H-reflex increase did not occur significantly earlier than the onset of the SOL EMG increase (127 ± 5 ms). An important inter-subject variability was observed for the onset of H-reflex modulation with respect to EMG response for each direction of tilt, but this variability could not be explained by the subject’s height. Taken together, the results establish the time course of change in SOL H-reflex excitability and its relation to the increase and decrease in SOL EMG activity during forward and backward tilts. The data presented here also suggest that balance mechanisms may differ between forward and backward tilts.

Introduction Les personnes ayant une lesion de la moelle epiniere incomplete (LMEi) presentent des reactions posturales alterees. Pour comprendre les mecanismes neuronaux sous-jacents, la modulation de l’excitabilite spinale lors de perturbations a ete analysee. Materiel et methodes Dix hommes ayant une LMEi [chronique ; Resultats L’aire de l’ellipse etait superieure dans le groupe LMEi lors de P-Av (p = 0,017). Cependant, aucune difference n’etait observee concernant l’Ex-CdP. En P-Ar, les latences d’inhibition du SOL (p = 0,016) et de facilitation du TA (p = 0,002) etaient plus longues dans le groupe LMEi. En P-Av, les latences des facilitations du SOL (p Discussion/conclusion La modulation de l’excitabilite spinale lors de desequilibres serait diminuee et retardee chez les individus LMEi. Ceci pourrait contribuer a l’alteration des reactions posturales observees.

Introduction La stimulation vestibulaire galvanique (GVS) est utilisee pour evaluer l’integrite du systeme vestibulaire et ameliorer notre comprehension des mecanismes de l’equilibre, mais les reponses evoquees montrent une grande variabilite interindividuelle, ce qui rend la comprehension du role du systeme vestibulaire difficile. L’objectif est de developper un protocole identifiant un seuil objectif (T) pour la GVS afin de limiter cette variabilite. Materiels et methodes Dix-huit sujets sains droitiers etaient debout sur une plateforme de force, les yeux fermes, la tete vers l’avant. L’acceleration de la tete etait enregistree lorsque la GVS (200 ms) etait appliquee a des intensites de 1–4,5 mA : – des courbes de recrutement ont ete generees afin de determiner un seuil. Puis, les participants ont ete stimules a differentes intensites relatives au seuil. Mesures ; – aire de l’ellipse de confiance (AE) a 95 % ; – vitesse de deplacement du centre de pression (CoP) ; – activite electromyographique du soleaire (EMG SOL). Resultats (1) Un seuil a ete determine pour chaque sujet base sur l’acceleration de la tete. (2) L’AE etait plus grande a 1,5 T (p = 0,007) et a 1 T (p = 0,038) compare a 0,5 T. (3) L’amplitude de la vitesse de deplacement du CoP dans l’axe mediolateral etait plus grande a 1,5 T (p = 0,002), 1 T (p = 0,008) et 0,75 T (p = 0,03) compare a 0,5 T. (4) L’intensite de stimulation ne correlait pas avec l’amplitude des reponses EMG du SOL. Discussion Un seuil objectif vestibulaire peut etre identifie par un accelerometre. Les reponses vestibulaires mesurees par l’AE et le CoP sont proportionnelles aux intensites relatives au seuil.

Study Design This is a focused review article. Objectives To identify important concepts in lower extremity (LE) assessment with a focus on locomotor outcomes and provide guidance on how existing outcome measurement tools may be best used to assess experimental therapies in spinal cord injury (SCI). The emphasis lies on LE outcomes in individuals with complete and incomplete SCI in Phase II-III trials. Methods This review includes a summary of topics discussed during a workshop focusing on LE function in SCI, conceptual discussion of corresponding outcome measures and additional focused literature review. Results There are a number of sensitive, accurate, and responsive outcome tools measuring both quantitative and qualitative aspects of LE function. However, in trials with individuals with very acute injuries, a baseline assessment of the primary (or secondary) LE outcome measure is often not feasible. Conclusion There is no single outcome measure to assess all individuals with SCI that can be used to monitor changes in LE function regardless of severity and level of injury. Surrogate markers have to be used to assess LE function in individuals with severe SCI. However, it is generally agreed that a direct measurement of the performance for an appropriate functional activity supersedes any surrogate marker. LE assessments have to be refined so they can be used across all time points after SCI, regardless of the level or severity of spinal injury. Sponsors Craig H. Neilsen Foundation, Spinal Cord Outcomes Partnership Endeavor.

Diffusion tensor imaging has been used in a number of spinal cord studies, but severe distortions caused by susceptibility induced field inhomogeneities limit its applicability to investigate small volumes within acceptable acquisition times. A way to evaluate image distortions is to map the point spread function of the voxel intensity in a reference scan. In this study, the point spread function was mapped for an echo-planar imaging sequence in the human cervical spinal cord with isotropic resolution and large field of view. Correction with the point spread function map improved anatomical consistency, and full cervical tractography was thereby possible from a C1 seed region in healthy controls and one individual with spinal cord injury. It is suggested that point spread function mapping of the spinal cord can be used in combination with sequence-based methods for reduction of susceptibility artifacts or in high-field imaging settings where off-resonance effects are pronounced. Magn Reson Med, 2013. © 2012 Wiley Periodicals, Inc.

Force field adaptation of locomotor muscle activity is one way of studying the ability of the motor control networks in the brain and spinal cord to adapt in a flexible way to changes in the environment. Here, we investigate whether the corticospinal tract is involved in this adaptation. We measured changes in motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in the tibialis anterior (TA) muscle before, during, and after subjects adapted to a force field applied to the ankle joint during treadmill walking. When the force field assisted dorsiflexion during the swing phase of the step cycle, subjects adapted by decreasing TA EMG activity. In contrast, when the force field resisted dorsiflexion, they increased TA EMG activity. After the force field was removed, normal EMG activity gradually returned over the next 5 min of walking. TA MEPs elicited in the early swing phase of the step cycle were smaller during adaptation to the assistive force field and larger during adaptation to the resistive force field. When elicited 5 min after the force field was removed, MEPs returned to their original values. The changes in TA MEPs were larger than what could be explained by changes in background TA EMG activity. These effects seemed specific to walking, as similar changes in TA MEP were not seen when seated subjects were tested during static dorsiflexion. These observations suggest that the corticospinal tract contributes to the adaptation of walking to an external force field.

Recovery of function following lesions in the nervous system requires adaptive changes in surviving circuitries. Here we investigate whether changes in cerebral activation are correlated to spinal cord atrophy and recovery of functionality in individuals with incomplete spinal cord injury (SCI). 19 chronic SCI individuals and 7 age-comparable controls underwent functional magnetic resonance imaging (fMRI) while performing rhythmic dorsiflexion of the ankle. A significant negative correlation was found between the activation in the ipsilateral motor (M1) and bilateral premotor cortex (PMC) on one hand and the functional ability of the SCI participants measured by the clinical motor score on the other. There was no significant correlation between activation in any other cerebral area and the motor score. Activation in ipsilateral somatosensory cortex (S1), M1 and PMC was negatively correlated to the width of the spinal cord in the left–right direction, where the corticospinal tract is located, but not in the antero-posterior direction. There was a tendency for a negative correlation between cerebral activation in ipsilateral S1, M1 and PMC and the amplitude of motor evoked potentials in the tibialis anterior muscle elicited by transcranial magnetic stimulation, but this did not reach statistical significance. There was no correlation between motor score or spinal cord dimensions and the volume of the cortical motor areas. The observations show that lesion of descending tracts in the lateral part of the spinal cord results in increased activation in ipsilateral motor and sensory areas, which may help to compensate for the functional deficit following SCI.

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.

When we walk, our arm muscles show rhythmic activity suggesting that the central nervous system contributes to the swing of the arms. The purpose of the present study was to investigate whether corticospinal drive plays a role in the control of arm muscle activity during human walking. Motor evoked potentials (MEPs) elicited in the posterior deltoid muscle (PD) by transcranial magnetic stimulation (TMS) were modulated during the gait cycle in parallel with changes in the background EMG activity. There was no significant difference in the size of the MEPs at a comparable level of background EMG during walking and during static PD contraction. Short latency intracortical inhibition (SICI; 2 ms interval) studied by paired-pulse TMS was diminished during bursts of PD EMG activity. This could not be explained only by changes in background EMG activity and/or control MEP size, since SICI showed no correlation to the level of background EMG activity during static PD contraction. Finally, TMS at intensity below the threshold for activation of corticospinal tract fibres elicited a suppression of the PD EMG activity during walking. Since TMS at this intensity is likely to only activate intracortical inhibitory interneurones, the suppression is in all likelihood caused by removal of a corticospinal contribution to the ongoing EMG activity. The data thus suggest that the motor cortex makes an active contribution, through the corticospinal tract, to the ongoing EMG activity in arm muscles during walking.

The present paper reviews aspects of locomotor sensorimotor interactions by focussing on work performed in spinal cats. We provide a brief overview of spinal locomotion and describe the effects of various types of sensory deprivations (e.g. rhizotomies, and lesions of muscle and cutaneous nerves) to highlight the spinal neuroplasticity necessary for adapting to sensory loss. Recent work on plastic interactions between reflex pathways that could be responsible for such plasticity, in particular changes in proprioceptive and cutaneous pathways that occur during locomotor training of spinal cats, is discussed. Finally, we describe how stimulation of some sensory inputs via various limb manipulations or intraspinal electrical stimulation can affect the expression of spinal locomotion. We conclude that sensory inputs are critical not only for locomotion but also that changes in the efficacy of sensory transmission and in the interactions between sensory pathways could participate in the normalization of locomotion after spinal and/or peripheral lesions.

Human bipedal gait requires supraspinal control and gait is consequently severely impaired in most persons with spinal cord injury (SCI). Little is known of the contribution of lesion of specific descending pathways to the clinical manifestations of gait deficits. Here, we assessed transmission in descending pathways using imaging and electrophysiological techniques and correlated them with clinical measures of impaired gait in persons with SCI. Twenty-five persons with SCI participated in the study. Functional assessment of gait included the Walking Index for Spinal Cord Injury (WISCI), the Timed-Up and Go (TUG), the 6-Min Walking Test (6MWT), and the maximal treadmill gait speed. Balance was evaluated clinically by the Berg Balance Scale (BBS). The amplitude of tibialis anterior (TA) motor-evoked potentials (MEPs) at rest elicited by transcranial magnetic stimulation as a measure of corticospinal transmission showed a moderately good correlation with all clinical measures (r(2)~0.5), whereas the latency of the MEPs showed less good correlation (r(2)~0.35). Interestingly, the MEP amplitude was correlated to atrophy in the ventrolateral rather than the dorsolateral section of the spinal cord where the main part of the corticospinal tract is located. TA intramuscular coherence in the beta and gamma frequency range has been suggested to reflect corticospinal transmission and was, consistent with this, found to be correlated to atrophy in the dorsolateral and ventrolateral sections of the spinal cord. Coherence was found to correlate to all clinical measures to the same extent as the MEP amplitude. The latency and duration of medium-latency responses in the soleus muscle to galvanic stimulation as measures of vestibulospinal transmission showed very good correlation to BBS (r(2)=-0.8) and moderately good correlation to the assessments of gait function (r(2)~0.4). 6MWT and gait speed were correlated to atrophy of the lateral sections of the spinal cord bilaterally, whereas BBS was correlated to atrophy of both lateral and ventral sections of the spinal cord. No significant correlation was observed between the electrophysiological tests of corticospinal and vestibulospinal transmission. Combination of different electrophysiological and anatomical measures using best subset regression analysis revealed improved prediction of gait ability, especially in the case of WISCI. These findings illustrate that lesion of corticospinal and vestibulospinal pathways makes different contributions to impaired gait ability and balance following SCI and that no single electrophysiological or anatomical measure provide an optimal prediction of clinical gait and balance disability. We suggest using a combination of anatomical and electrophysiological measures when evaluating spinal cord integrity following SCI.

This paper reviews findings on the adaptive changes of locomotion in cats after spinal cord or peripheral nerve lesions. From the results obtained after lesions of the ventral/ventrolateral pathways or the dorsal/dorsolateral pathways, we conclude that with extensive but partial spinal lesions, cats can regain voluntary quadrupedal locomotion on a treadmill. Although tract-specific deficits remain after such lesions, intact descending tracts can compensate for the lesioned tracts and access the spinal network to generate voluntary locomotion. Such neuroplasticity of locomotor control mechanisms is also demonstrated after peripheral nerve lesions in cats with intact or lesioned spinal cords. Some models have shown that recovery from such peripheral nerve lesions probably involves changes at the supra spinal and spinal levels. In the case of somesthesic denervation of the hindpaws, we demonstrated that cats with a complete spinal section need some cutaneous inputs to walk with a plantigrade locomotion, and that even in this spinal state, cats can adapt their locomotion to partial cutaneous denervation. Altogether, these results suggest that there is significant plasticity in spinal and supraspinal locomotor controls to justify the beneficial effects of early proactive and sustained locomotor training after central (Rossignol and Barbeau 1995; Barbeau et al. 1998) or peripheral lesions.Key words: spinal lesions, nerve lesions, locomotion, neuroplisticity, locomotor training.

In most species, locomotor function beneath the level of a spinal cord lesion can be restored even if the cord is completely transected. This suggests that there is, within the spinal cord, an autonomous network of neurons capable of generating a locomotor pattern independently of supraspinal inputs. Recent studies suggest that several physiological and neurochemical changes have to occur in the neuronal networks located caudally to the lesion to allow the expression of spinal locomotion. Some evidence of this plasticity will be addressed in this review. In addition, original data on the functional organisation of the lumbar spinal cord will also be presented. Recent works in our lab show that segmental responsiveness of the spinal cord of the cat to locally micro-injected drugs in different lumbar segments, in combination with complete lesions at various level of the spinal cord, suggest a rostro-caudal organisation of spinal locomotor control. Moreover, the integrity of midlumbar segments seems to be crucial for the expression of spinal locomotion. These data suggest that the regions of critical importance for locomotion can be confined to a restricted portion of the spinal cord. Later, these midlumbar segments could be targeted by electrical stimulation or grafts to improve recovery of function. Understanding the changes in spinal cord neurophysiology and neurochemistry after a lesion is of critical importance to the improvement of treatments for locomotor rehabilitation in spinal-cord-injured patients.

Maximum toe elevation during walking is an objective measure of foot drop and reflects the impairment of the corticospinal tract (CST) in persons with spinal cord injury (SCI). To determine if this measurement is functionally relevant to ambulatory abilities, we correlated maximum toe elevation with clinical physiotherapy tests. Cross-sectional study, laboratory and clinical settings. A total of 24 individuals with SCI (American Spinal Injury Association (ASIA) Impairment Scale D) were recruited. Maximum toe elevation during the swing phase of treadmill gait was measured with a kinematic system. CST function was assessed in a sitting position by measuring the motor-evoked potentials (MEPs) induced in tibialis anterior muscle with transcranial magnetic stimulation over the motor cortex. Clinical tests performed were 10-m and 6-min walk test (6MWT), Timed-Up and Go (TUG), Walking Index for Spinal Cord Injury, Berg Balance Scale, Lower Extremity Motor Score (LEMS) and sensory score of the L4, L5 and S1 dermatomes. Participants with lower toe elevation during gait walked at a slower speed, took more time to perform the TUG test, and covered a shorter distance in the 6MWT. They also scored lower on the LEMS and showed impaired superficial sensitivity of the dermatomes around the ankles. Few correlations were observed between CST function and clinical tests, but the presence of MEP at rest was indicative of faster speed and longer distance in the 6MWT. These results indicate that maximum toe elevation, which is directly correlated with CST impairment, is functionally relevant as it also correlates with timed clinical tests, LEMS and sensory scores.

Given the inherent mechanical complexity of human bipedal locomotion, and that complete spinal cord lesions in human leads to paralysis with no recovery of gait, it is often suggested that the corticospinal tract (CST) has a more predominant role in the control of walking in humans than in other animals. However, what do we actually know about the contribution of the CST to the control of gait? This chapter will provide an overview of this topic based on the premise that a better understanding of the role of the CST in gait will be essential for the design of evidence-based approaches to rehabilitation therapy, which will enhance gait ability and recovery in patients with lesions to the central nervous system (CNS). We review evidence for the involvement of the primary motor cortex and the CST during normal and perturbed walking and during gait adaptation. We will also discuss knowledge on the CST that has been gained from studies involving CNS lesions, with a particular focus on recent data acquired in people with spinal cord injury.

Locomotion is a very robust motor pattern which can be optimized after different types of lesions to the central and/or peripheral nervous system. This implies that several plastic mechanisms are at play to re-express locomotion after such lesions. Here, we review some of the key observations that helped identify some of these plastic mechanisms. At the core of this plasticity is the existence of a spinal central pattern generator (CPG) which is responsible for hindlimb locomotion as observed after a complete spinal cord section. However, normally, the CPG pattern is adapted by sensory inputs to take the environment into account and by supraspinal inputs in the context of goal-directed locomotion. We therefore also review some of the sensory and supraspinal mechanisms involved in the recovery of locomotion after partial spinal injury. We particularly stress a recent development using a dual spinal lesion paradigm in which a first partial spinal lesion is made which is then followed, some weeks later, by a complete spinalization. The results show that the spinal cord below the spinalization has been changed by the initial partial lesion suggesting that, in the recovery of locomotion after partial spinal lesion, plastic mechanisms within the spinal cord itself are very important.

Given the inherent mechanical complexity of human bipedal locomotion, and that complete spinal cord lesions in human leads to paralysis with no recovery of gait, it is often suggested that the corticospinal tract (CST) has a more predominant role in the control of walking in humans than in other animals. However, what do we actually know about the contribution of the CST to the control of gait? This chapter will provide an overview of this topic based on the premise that a better understanding of the role of the CST in gait will be essential for the design of evidence-based approaches to rehabilitation therapy, which will enhance gait ability and recovery in patients with lesions to the central nervous system (CNS). We review evidence for the involvement of the primary motor cortex and the CST during normal and perturbed walking and during gait adaptation. We will also discuss knowledge on the CST that has been gained from studies involving CNS lesions, with a particular focus on recent data acquired in people with spinal cord injury.

Locomotion is a very robust motor pattern which can be optimized after different types of lesions to the central and/or peripheral nervous system. This implies that several plastic mechanisms are at play to re-express locomotion after such lesions. Here, we review some of the key observations that helped identify some of these plastic mechanisms. At the core of this plasticity is the existence of a spinal central pattern generator (CPG) which is responsible for hindlimb locomotion as observed after a complete spinal cord section. However, normally, the CPG pattern is adapted by sensory inputs to take the environment into account and by supraspinal inputs in the context of goal-directed locomotion. We therefore also review some of the sensory and supraspinal mechanisms involved in the recovery of locomotion after partial spinal injury. We particularly stress a recent development using a dual spinal lesion paradigm in which a first partial spinal lesion is made which is then followed, some weeks later, by a complete spinalization. The results show that the spinal cord below the spinalization has been changed by the initial partial lesion suggesting that, in the recovery of locomotion after partial spinal lesion, plastic mechanisms within the spinal cord itself are very important.

Cross-sectional descriptive analysis of magnetic resonance imaging (MRI) and clinical outcome. The aim of this study was to present anatomically consistent and independent spinal cord atrophy measures based on standard MRI material and analyze their specific relations to sensory and motor outcome in individuals with chronic incomplete spinal cord injury (SCI). Danish study on human SCI. We included 19 individuals with chronic incomplete SCI and 16 healthy controls. Participants underwent MRI and a neurological examination including sensory testing for light touch and pinprick, and muscle strength. Antero–posterior width (APW), left–right width (LRW) and cross-sectional spinal cord area (SCA) were extracted from MRI at the spinal level of C2. The angular variation of the spinal cord radius over the full circle was also extracted and compared with the clinical scores. The motor score was correlated to LRW and the sensory scores were correlated to APW. The scores correlated also well with decreases in spinal cord radius in oblique angles in coherent and non-overlapping sectors for the sensory and motor qualities respectively. APW and LRW can be used to assess sensory and motor function independently. The finding is corresponding well with the respective locations of the main sensory and motor pathways.

Intraspinal microstimulation (ISMS) through a single microelectrode can induce locomotion in cats spinalized at T131 wk before (untrained) or after 3–5 wk of treadmill training. Here we study the optimal parameters of ISMS and the characteristics of locomotion evoked. ISMS was applied in the dorsal region of segments L3–S1at different lateralities (midline to 2.5 mm) and after an intravenous injection of clonidine (noradrenergic agonist). Kinematics and electromyographic recordings were used to characterize locomotion. ISMS could induce a bilateral locomotor pattern similar to that obtained with perineal stimulation, and the characteristics of locomotion varied according to the spinal segment stimulated. Mechanisms by which ISMS could evoke locomotion were then investigated by stimulating, inactivating, or lesioning different spinal structures. Dorsal root stimulation (DRS), just like ISMS, could evoke a variety of ipsi- and bilateral nonlocomotor movements as well as locomotor responses. This suggests that sensory afferent pathways are involved in the production of locomotion by ISMS. Microinjections of yohimbine (noradrenergic antagonist) in L3and L4segments or a complete second spinal lesion at L3–L4abolished all locomotor activity evoked by ISMS applied at more caudal segments. Progressive dorsoventral spinal lesions at L3or L4and restricted ventral lesions at L4further suggest that the integrity of the ventral or ventrolateral funiculi as well as the L3–L4segments are critical for the induction of locomotion by ISMS at L5to S1or by DRS at these caudal segments.

As a preliminary step to using intraspinal microstimulation (ISMS) for rehabilitation purposes, the distribution of various types of hindlimb responses evoked by ISMS in spinal cats (T13) is described. The responses to ISMS applied through a single electrode was assessed, before and after an intravenous injection of clonidine (noradrenergic agonist), using kinematics and electromyographic recordings in subacute (5–7 days, untrained) or chronic (3–5 wk trained on a treadmill) spinal cats. ISMS was applied in the dorsal, intermediate and ventral areas of segments L3–L7, from midline to 3 mm laterally. Uni- and bilateral non-locomotor responses as well as rhythmical locomotor responses were evoked. In the subacute cats, ipsilateral flexion was elicited in the dorsal region of L3–L7, whereas ipsilateral extension was evoked more ventrally and mainly in the caudal segments. Dorsal stimuli could induce ipsilateral flexion followed by ipsilateral extension. Sites inducing bilateral flexion and bilateral extension were similarly distributed to those evoking ipsilateral flexion and extension in the rostrocaudal axis but were evoked from more medial sites. Ipsilateral flexion with crossed extension was evoked from intermediate and ventral zones of all segments and lateralities. Unilateral ipsilateral locomotion was rarely observed. Contralateral locomotion was more frequent and mainly evoked medially, whereas bilateral locomotion was evoked exclusively from dorsal regions. With some exceptions, those distribution gradients were similar in the four conditions (subacute, chronic, pre- and postclonidine), but the proportion of each response could vary. The distribution of ISMS-evoked responses is discussed as a function of known localization of interneurons and motoneurons.

The development of limb motor innervation was studied in the opossum Monodelphis domestica, a marsupial born with immature mobile forelimbs and immobile hindlimbs. Choline acetyltransferase (ChAT), the synthesis enzyme of acetylcholine, was evidenced on sections of the spinal enlargements, and the protein that transports acetylcholine (VAChT) on limb sections. In newborn, ChAT immunolabeling occurred in small, undifferentiated neurons of the ventral horn, presumably motoneurons, and intermediate and dorsal gray matter, and in the presumptive white matter, all less abundant at lumbosacral than brachial levels. Scant immunolabeling for VAChT marked small terminal-looking profiles, presumably growth cones or immature neuromuscular junctions, decreasing proximodistally in each limb and being less abundant in hindlimbs than forelimbs; it was absent distally in the foot where no muscle tissue was formed. ChAT labeling disappeared from the white matter within 1 week while cholinergic neurons increased in number and size. Motoneurons segregated in a medial and lateral group by 4–5 weeks. VAChT-labeled profiles increased in number and size and they flattened along a proximodistal gradient within each limb, but later in the hindlimbs than in the forelimbs. Labeling appeared in distal foot muscle at 1 week. The density, size, and shape of terminals became comparable in all segments of a given limb by 3–4 weeks. Their number and size increased, and by 8 weeks, they clustered in 3 or 4 along muscle fibers. Thus, limb motor innervation develops largely postnatally in the opossum, along rostrocaudal and proximodistal gradients. Its timecourse is compared to the development of motor behaviors.

After a spinalization at the most caudal thoracic spinal segment, the cat can recover locomotion of the hindlimbs when they are placed on a moving treadmill. This chapter summarizes some of the determinants of such a dramatic recovery of motor function. Fundamental to this recovery is undoubtedly the genetically based spinal locomotor generator, which provides an essential rhythmicity to spinal motoneurons and hence the musculature. Other factors are also important, however. Sensory feedback is essential for the correct expression of spinal locomotion because spinal cats, devoid of cutaneous feedback from the hindfeet, are incapable of plantar foot placement. The neurochemical environment also adapts to spinalization, i.e., the loss of all modulation by descending monoaminergic pathways. Post-transection spinal rhythmicity then becomes more dependent on glutamatergic mechanisms. Finally, we argue that the mid-lumbar spinal segments evolve to play a crucial role in the elaboration of spinal locomotion as their inactivation abolishes spinal locomotion. In summary, the above findings suggest that the recovery of spinal locomotion is determined by a number of factors, each of which must now be more fully understood in the ever-continuing effort to improve the rehabilitation of spinal-cord-injured subjects.

After a spinalization at the most caudal thoracic spinal segment, the cat can recover locomotion of the hindlimbs when they are placed on a moving treadmill. This chapter summarizes some of the determinants of such a dramatic recovery of motor function. Fundamental to this recovery is undoubtedly the genetically based spinal locomotor generator, which provides an essential rhythmicity to spinal motoneurons and hence the musculature. Other factors are also important, however. Sensory feedback is essential for the correct expression of spinal locomotion because spinal cats, devoid of cutaneous feedback from the hindfeet, are incapable of plantar foot placement. The neurochemical environment also adapts to spinalization, i.e., the loss of all modulation by descending monoaminergic pathways. Post-transection spinal rhythmicity then becomes more dependent on glutamatergic mechanisms. Finally, we argue that the mid-lumbar spinal segments evolve to play a crucial role in the elaboration of spinal locomotion as their inactivation abolishes spinal locomotion. In summary, the above findings suggest that the recovery of spinal locomotion is determined by a number of factors, each of which must now be more fully understood in the ever-continuing effort to improve the rehabilitation of spinal-cord-injured subjects.

Publisher Summary This chapter discusses the changes occurring in the spinal cord that may lead to the re-expression of motor patterns such as hind-limb locomotion. The chapter reviews some aspects of locomotor training with and without the use of drugs, the evolution of pharmacological receptors below the level of lesion. It also discusses the role of various neurotransmitter systems before and after spinalization, the key role played by certain rostral lumbar segments of the spinal cord in the generation of locomotion, and the necessity of cutaneous inputs from the pads for the expression of spinal locomotion. The chapter discusses the recovery of locomotion in adult spinal cats is probably the result of numerous plastic changes occurring at the level of the sensory afferents, cellular properties of neurons and receptors for neurotransmitters. The spinal cord is a complex laminar and segmental structure.

Vesicular acetylcholine transporter (VAChT) was revealed immunohistochemically in light microscopy on hindlimb sections of developing opossums, Monodelphis domestica. In the immobile hindlimbs of the newborn, which comprise cartilaginous bones and loose, unstriated myofibers, scant immunolabeled nerve segments and small spherical terminals, presumably growth cones or immature neuromuscular junctions, are found in the muscle tissue of the thigh, leg and proximal foot, decreasing in number and size proximodistally. When the hindlimbs start moving at 1 week, terminals are more numerous and larger, still decreasing proximodistally, and occur in the newly formed interosseous foot muscles. At 4 weeks, when the hindlimbs start supporting weight and quadrupedal locomotion appears, terminals are more numerous, flattened and in comparable size and density in thigh, leg and foot muscles. By 7 weeks, large and completely flat terminals are observed in groups of 3 to 4 at regular intervals along muscle fibers. VAChT expression develops largely postnatally in the opossum hindlimbs, along a proximodistal gradient that parallels somatic and reflex development.