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The precise role of cognitive control on optic flow processing during locomotion has rarely been investigated. Therefore, this study aimed to determine whether coping with unreliable visual inputs during walking requires attentional resources. Twenty-four healthy young adults walked on an instrumented treadmill in a virtual environment under two optic flow conditions: normal (NOF) and perturbed (POF, continuous mediolateral pseudo-random oscillations). Each condition was performed under single-task and dual-task conditions of increasing difficulty (1-, 2-, 3-back). In all conditions, subjective mental workload was estimated (raw NASA-TLX). For kinematic variables, mean, standard deviation, statistical persistence and step-to-step error correction were computed from gait time series in mediolateral and anteroposterior directions. For EMG variables ofsoleusandgluteus medius, the full width at half maximum and the variance ratio were calculated. Performance on N-back tasks was assessed using mean reaction time and d-prime. Cognitive performance was not affected by simultaneous walking in any optic flow condition. Gait variability was altered under POF compared to NOF, so that young adults sought to counteract those perturbations by adopting an effortful gait control strategy, independently of concurrent working memory (WM) load. Increasing WM load led changes first at the neuromuscular level, then at the behavioral level, with a prioritization of gait control in the mediolateral direction. Interestingly, dual-tasking lowered the effects of POF but in the anteroposterior direction only. These findings and their theoretical implications provide valuable insight into the complex interaction effects of cognitive and visual constraints on gait control during treadmill walking.Highlights-Cognitive performance was preserved during DTW regardless of optic flow condition.-ML POF under DTW increased subjective mental workload.-Young adults counteracted ML POF by adopting an effortful gait control strategy.-DTW led them to prioritize gait control in the ML direction over AP direction.-Concurrent WM load attenuated ML POF effect on step velocity variability.

Few studies have examined the pathways linking personality to cognition. This study aimed to examine whether measures of physical performance (gait speed, peak expiratory flow (PEF), and grip strength) mediated the association between five-factor model personality traits and cognition (memory performance, subjective memory, and informant-rated cognition). Participants were aged 57 to 95 years from the Health and Retirement Study (HRS, N = 4,109) and the English Longitudinal Study of ageing (ELSA, N = 3,584). In HRS, personality and demographic factors were assessed in 2008/2010, physical performance in 2012/2014, and memory performance and subjective memory in 2016/2018. Informant-rated cognition was obtained in 2016 for an HRS subsample. In ELSA, personality and demographic factors were assessed in 2010/2011, physical performance in 2012/2013, and objective and subjective memory in 2014/2015. Informant-rated cognition was obtained in 2018 for an ELSA subsample. With a few exceptions, replicable patterns of mediation were found across HRS and ELSA. Slower gait speed partially mediated the association between higher neuroticism, lower conscientiousness and worse scores on all three cognitive measures (memory performance, subjective memory, and informant-rated cognition). Slower gait also partially mediated the association between openness and both objective and subjective memory. There was less replicable evidence for a mediating role of PEF and grip strength. The present study advances knowledge on the pathways linking personality to cognition in older adults and supports the hypothesis that personality associations with better physical function can help support healthy cognitive aging.

KEY POINTS During moderate and high levels of quadriceps force production, the ipsilateral motor cortex is concomitantly activated with the contralateral motor cortex throughout the corpus callosum to generate the motor command. Chronic obstructive pulmonary disease (COPD) patients display a structurally impaired corpus callosum that may explain the reduced motor command in this population, which in turn contributes to COPD-related muscle weakness of the knee extensors. The study aimed to determine whether bilateral connectivity was impaired and ipsilateral activation was lowered during unilateral strength production of the knee extensors. Our results indicate impaired bilateral connectivity but preserved ipsilateral activation in patients during unilateral isometric contractions of 50% of maximum voluntary strength. The preservation of ipsilateral activation during force production despite impaired bilateral connectivity is consistent with a reorganization of bilateral motor network function that drives unilateral strength production. ABSTRACT The contralateral primary motor cortex (M1) is not the only brain area implicated in motor command generation. During moderate and high levels of quadriceps force production, the ipsilateral M1 is concomitantly activated. Such activation is mediated by the corpus callosum, the main component of bilateral connectivity. Structural damage to the corpus callosum has been observed in chronic obstructive pulmonary disease (COPD) patients, which might reduce ipsilateral activation and contribute to the lower motor command associated with COPD muscle weakness. We thus aimed to determine whether bilateral connectivity and ipsilateral activation were impaired in COPD. Twenty-two COPD patients and 21 healthy age-matched controls were evaluated by transcranial magnetic stimulation, at rest and during 50% of maximal voluntary isometric contraction (MVIC) of the dominant vastus lateralis muscle. Bilateral connectivity was determined by the ipsilateral silent period (iSP) during 50% MVIC. Ipsilateral activation was determined as the increase in ipsilateral excitability from rest to 50% MVIC. As expected, COPD patients had significantly lower MVIC (-25%, p = 0.03). These patients also showed a significantly lower iSP (-53%, p

Voluntary force production requires that the brain produces and transmits a motor command to the muscles. It is widely acknowledged that motor commands are executed from the primary motor cortex (M1) located in the contralateral hemisphere. However, involvement of M1 located in the ipsilateral hemisphere during moderate to high levels of unilateral muscle contractions (>30% of the maximum) has been disclosed in recent years. This phenomenon has been termed cross-activation. The activation of the ipsilateral M1 relies on complex inhibitory and excitatory interhemispheric interactions mediated via the corpus callosum and modulated according to the contraction level. The regulatory mechanisms underlying these interhemispheric interactions, especially excitatory ones, remain vague, and contradictions exist in the literature. In addition, very little is known regarding the possibility that other pathways could also mediate the cross-activation. In the present review, we will therefore summarize the concept of cross-activation during unilateral voluntary muscle contraction and explore the associated mechanisms and other nervous system pathways underpinning this response. A broader knowledge of these mechanisms would consequently allow a better comprehension of the motor system as a whole, as distant brain networks working together to produce the motor command. Refereed/Peer-reviewed

The crossed-facilitation (CF) effect refers to when motor-evoked potentials (MEPs) evoked in the relaxed muscles of one arm are facilitated by contraction of the opposite arm. The aim of this study was to determine whether high-definition transcranial direct-current stimulation (HD-tDCS) applied to the right primary motor cortex (M1) controlling the left contracting arm [50% maximum voluntary isometric contraction (MVIC)] would further facilitate CF toward the relaxed right arm. Seventeen healthy right-handed subjects participated in an anodal and cathodal or sham HD-tDCS session of the right M1 (2 mA for 20 min) separated by at least 48 h. Single-pulse transcranial magnetic stimulation (TMS) was used to elicit MEPs and cortical silent periods (CSPs) from the left M1 at baseline and 10 min into and after right M1 HD-tDCS. At baseline, compared with resting, CF (i.e., right arm resting, left arm 50% MVIC) increased left M1 MEP amplitudes (+97%) and decreased CSPs (−11%). The main novel finding was that right M1 HD-tDCS further increased left M1 excitability (+28.3%) and inhibition (+21%) from baseline levels during CF of the left M1, with no difference between anodal and cathodal HD-tDCS sessions. No modulation of CSP or MEP was observed during sham HD-tDCS sessions. Our findings suggest that CF of the left M1 combined with right M1 anodal or cathodal HD-tDCS further facilitated interhemispheric interactions during CF from the right M1 (contracting left arm) toward the left M1 (relaxed right arm), with effects on both excitatory and inhibitory processing. NEW & NOTEWORTHY This study shows modulation of the nonstimulated left M1 by right M1 HD-tDCS combined with crossed facilitation, which was probably achieved through modulation of interhemispheric interactions.

Repeated transcranial magnetic stimulation (rTMS) is a well-known clinical neuromodulation technique, but transcranial direct-current stimulation (tDCS) is rapidly growing interest for neurorehabilitation applications. Both methods (contralesional hemisphere inhibitory low-frequency: LF-rTMS or lesional hemisphere excitatory anodal: a-tDCS) have been employed to modify the interhemispheric imbalance following stroke. The aim of this pilot study was to compare aHD-tDCS (anodal high-definition tDCS) of the left M1 (2 mA, 20 min) and LF-rTMS of the right M1 (1 Hz, 20 min) to enhance excitability and reduce inhibition of the left primary motor cortex (M1) in five healthy subjects. Single-pulse TMS was used to elicit resting and active (low level muscle contraction, 5% of maximal electromyographic signal) motor-evoked potentials (MEPs) and cortical silent periods (CSPs) from the right and left extensor carpi radialis muscles at Baseline, immediately and 20 min (Post-Stim-20) after the end of each stimulation protocol. LF-rTMS or aHD-tDCS significantly increased right M1 resting and active MEP amplitude at Post-Stim-20 without any CSP modulation and with no difference between methods. In conclusion, this pilot study reported unexpected M1 excitability changes, which most likely stems from variability, which is a major concern in the field to consider.

During the production of high levels of strength (> 30% maximum), the recruitment of the ipsilateral primary motor cortex (M1) is driven by the contralateral M1 (Chiou et al., 2013). This recruitment is mediated by the corpus callosum, the main component of the interhemispheric connectivity. In COPD, structural damages of the corpus callosum were reported (Lahousse et al., 2013). Such alterations could reduce the ipsilateral activation and participate to the lower motor command in patients (Alexandre et al., 2014). Therefore, we aimed to determine whether interhemispheric connectivity and ipsilateral activation were decreased in COPD. Nineteen COPD patients (GOLD II-IV, aged 61.5 ± 7 yrs.) and 19 healthy age matched controls were evaluated at rest and during 50% of maximal voluntary contraction (MVC) of the dominant vastus lateralis by transcranial magnetic stimulation. The functional integrity of corpus callosum was determined by the ipsilateral silent period (iSP) during 50% MVC which is a classic index of interhemispheric connectivity. The ipsilateral activation was determined as the ratio between ipsilateral excitability measured during 50% MVC and at rest. COPD patients had significant lower MVC (91.8 ± 40.1 vs 122.2 ± 42.4 Nm, p = 0.04). The iSP was significantly reduced in patients (38.3 ± 13.4 vs 82.1 ± 22 ms, p Despite a reduced interhemispheric connectivity, the ipsilateral activation was not decreased in COPD. Thus, an ipsilateral flaw cannot be the underlying reason of the already described reduced motor command in COPD patients.

In an effort to increase the effectiveness of transcranial direct current stimulation (tDCS) application, new study designs are needed and a key issue is the timing of tDCS application in relation to a cognitive and/or motor task. In this opinion chapter we highlight two main types of study design encountered in the field of tDCS that could benefit the neuroergonomics community: “online” versus “offline” tDCS. Given that such types of design used in different ways can be confusing, we propose to use qualifiers for shedding light on the use of “online” and “offline” terminology in tDCS when related to a task, learning, and neuroimaging.

Introduction: Brain impairment, characterized by cognitive and motor alterations, is a frequent complication of COPD (Dodd et al., 2012, Heraud et al., 2018). Studies on functional alterations have reported decreased cortical activation and increased inhibitory network activity in the brain (Mohamed-Hussein et al., 2007, Alexandre et al., 2014). Many pharmacological treatments to manage anxiety in COPD increase this brain inhibitory activity (Di Lazzaro et al., 2006). This study therefore aimed to determine the prevalence of neuroleptic intake in COPD patients. Methods: COPD patients (406: 229 men/177 women, age: 65.23±9.9 years, BMI: 26.5±6.8, FEV1 (%th.): 51.98±21.44) enrolled in a pulmonary rehabilitation program (Cliniques du Souffle in Lodeve, Osseja or Riom-Es-Montagne, France) were retrospectively included. Results: Of these patients, 194 (47.8%) used neuroleptics. Benzodiazepines were the most prescribed class (29% of the 406 patients), followed by antidepressants (13.5%), antihistamines (12%), and opioids (7%). Of the 194 patients, 107 (55%) took two or more medications simultaneously. Conclusion: This study shows that neuroleptic use is very prevalent and may be an additional factor in explaining COPD-related brain disorder (cognitive impairment, reduced central motor drive, and motor control alterations). It also strengthens the role of non-pharmacological cares such as physical activity, as it can reduce anxiousness and thus neuroleptics intake, which would help to limit COPD brain impairment.

Introduction Facteur de pronostic, la faiblesse musculaire (FM) du quadriceps dans la BPCO est sous-diagnostiquee. Les societes savantes ont longtemps recommande le depistage exclusif de la FM chez les patients avec deficit de masse musculaire. Plusieurs etudes montrent un lien seulement modere entre force et masse musculaire ainsi que l’existence d’une faiblesse sans diminution de la masse. L’enjeu de ce travail etait de definir un indicateur plus precis pour le depistage de la FM a partir des evaluations de routine. Au vue, de la relation existante entre vitesse de marche (VM) et fonction musculaire [1] , le but etait d’identifier la mesure de VM la plus sensible pour depister la FM lors du test de marche de 6 min (TDM6). Methodes La force maximale isometrique volontaire (FMIV) du quadriceps, l’indice de masse maigre (IMM) et un TDM6 ont ete evalues chez 48 patients BPCO. A partir de la FMIV et de l’equation predictive de Seymour [2] , les patients etaient definis comme faible ou non faible. Lors du TDM6, la VM etait calculee selon differentes formules : moyenne par tour, moyenne du test moins les temps d’arrets, sur 4 m et 10 m depart arrete et 4 m depart lance. Les courbes ROC ont permis de determiner la meilleure methode diagnostique (plus grande aire sous la courbe) et de calculer la valeur seuil associee (meilleur compromis entre sensibilite et specificite). Resultats La VM moyenne par tour presentait la plus grande aire sous la courbe (0,83) avec une valeur seuil a 1,017 m.s−1 et une sensibilite de 78 %. L’IMM presentait l’aire sous la courbe la plus basse (0,68) pour une sensibilite de 61 %. Conclusion La determination de la VM (plus precisement une VM moyenne inferieure a 1,017 m.s−1) lors du TDM6 represente une alternative interessante a l’evaluation de la FMIV pour depister la FM des patients.

Introduction Des alterations corticales ont ete decrites chez les patients atteints de bronchopneumopathie chronique obstructive (BPCO). Ces patients presentent une sous-activation des aires motrices lors de la production volontaire de force [1] pouvant expliquer une partie de la faiblesse musculaire observee dans cette population. De plus, une suractivite des reseaux inhibiteux corticaux est classiquement rapportee chez ces patients [2] . Le but de cette etude etait de determiner s’il etait possible de compenser la suractivite inhibitrice chez les patients par une methode de neuromodulation corticale. Methodes Onze patients BPCO (GOLD II–IV) et neuf sujets sains apparies ont ete evalues lors de deux sessions passees aleatoirement a 48 h d’intervalle et impliquant une intervention par stimulation transcrânienne a courant continu (tDCS, 10 min/2 mA). La tDCS etait placee sur le cortex moteur primaire (M1) dominant selon deux modalites : anodale (intervention) et placebo. La force isometrique du quadriceps, les proprietes neuromusculaires, les potentiels moteurs evoques (MEP) et la periode de silence corticale (CSP) determines par stimulation magnetique transcrânienne ont ete evalues au niveau du muscle vastus lateralis avant et apres neuromodulation. Resultats L’intervention a significativement diminue la CSP ( p Fig. 1 ). Avant neuromodulation, cette CSP etait significativement plus importante chez les patients ( p Conclusion La suractivite inhibitrice presente chez les patients atteints de BPCO est donc reversible. Le reentrainement a l’effort, developpant le metabolisme oxydatif, pourrait theoriquement reduire l’activite glycolytique et son action sur les afferences metabosensibles inhibitrices. L’absence de gain de force doit etre relativisee car il est connu depuis peu que les effets optimaux de la tDCS sont retardes chez les personnes âgees.

Introduction La faiblesse musculaire dans la BPCO represente un enjeu clinique majeur. Les recommandations actuelles preconisent une evaluation systematique de la force, souvent difficile a mettre en place car necessitant une evaluation complementaire. La faiblesse musculaire reste alors sous-diagnostiquee. L’enjeu de ce projet etait de trouver une alternative pour le depistage des patients faibles sans envisager de test complementaire. Sachant qu’il existe une correlation positive entre vitesse de marche (VM) et faiblesse musculaire chez les sujets âges et vitesse de marche et pronostic vital chez les BPCO, nous avons cherche a definir 1) la formule de calcul de la VM au cours du test de marche de 6 minutes (TDM6) la plus precise pour depister les patients presentant une faiblesse musculaire par 2) la determination d’une valeur seuil de vitesse de marche. Methodes Au total, 48 patients BPCO ont realise une mesure de la Force maximale isometrique volontaire (FMIV) et un TDM6. A partir de la FMIV et de l’equation predictive de Seymour (2010), les patients etaient definis comme faible ou non faible. Lors du TDM6, nous avons calcule la VM selon differentes formules : sur 4 m et sur 10 m depart arrete, sur 4 m depart lance, vitesse moyenne d’un tour, et enfin vitesse moyenne du test moins les temps d’arrets. Nous avons ensuite eu recours au modele des « courbes ROC » (Receiver Operating Characteristic). A partir de cette methode, la determination des aires sous la courbe, nous a permis de comparer les performances diagnostiques des formules de determination de la VM precitees a notre methode de reference. Pour la formule la plus performante (ie donnant la plus grande aire sous la courbe), nous avons defini la valeur seuil de VM la plus discriminante (valeur definie comme le meilleur compromis entre la specificite et la sensibilite du test). Resultats L’aire sous la courbe la plus grande correspondait a la formule de VM moyenne moins les temps d’arret. La valeur seuil associee etait de 1,0167 m.s−1 ( Figure 1 ). Conclusion La determination de la VM au cours du TDM6 (et plus precisement une VM > a 1,0167 m.s−1) represente une alternative interessante a l’evaluation de la FMIV pour depister la faiblesse musculaire des patients BPCO.