IntroductionPrevious studies have linked endogenous pain modulation and corticospinal excitability (CSE), but methodological limitations and overlooking psychological factors may have constrained interpretations. This study aimed to evaluate the interaction between CSE excitability in different muscles and endogenous pain modulation, and to determine whether kinesiophobia and pain catastrophizing modulate this interaction.MethodsTwenty-one pain-free participants completed questionnaires on kinesiophobia and pain catastrophizing. Conditioned pain modulation (CPM) was used to assess endogenous pain modulation. Transcranial magnetic stimulation was used to assess the pain-induced modulation in CSE excitability, focusing on slope, S50 and the maximum response parameters of input-output curves (plateau) for the anterior deltoid (AD) and first dorsal interosseous (FDI) muscles, first in pain-free then in painful condition induced by the application of capsaicin cream to the shoulder.ResultsA significant correlation was found between the plateau of the AD input-output curves measured at baseline (pain-free condition) and CPM responses (rS = .56, p = 0.01), suggesting that higher maximal corticospinal output is associated with more effective endogenous pain modulation. Pain-induced changes in FDI slope and CPM responses were strongly correlated (rS = -.75, p < 0.001), indicating that individuals with the most effective endogenous pain inhibition mechanisms were those with the greatest increase in CSE. Finally, kinesiophobia was found to alter the association between pain-induced changes in CSE in AD (S50 shift) and CPM response, shedding new light on the influence of psychological factors on pain-induced CSE alterations and their link with descending pain inhibition.DiscussionThese findings underscore the complex interplay between corticospinal projections, pain modulation, and psychological factors, reinforcing the need for further investigation.
Most pain studies overlook the relationship between corticomotor function changes and coordinated muscle patterns in voluntary movement. A pre-post study was performed to investigate relationships between changes in corticospinal excitability (CSE) and spatial changes in muscle coordination in response to pain. Methods: Thirty pain-free participants performed an upper limb pointing task in pain-free then experimental painful conditions. Transcranial magnetic stimulation was used to assess CSE via the deltoid muscle input-output curves (slope, plateau and S50). Electromyography was used to record trapezius and deltoid muscle activity. Spatial adaptations of muscle coordination to pain were assessed using non-negative matrix factorization (NNMF), comparing the norm of coordination pattern vectors between pain and no-pain conditions, as well as the cosine of the angle between these vectors. Correlations were examined among pain-induced changes in CSE and muscle coordination. Results: Correlations revealed associations between pain-induced S50 change and both pain-induced cosine and norm changes (rS = 0.43; p = 0.05 for both). Additionally, a correlation was found between pain-induced changes in the coordination pattern's norm and both the IO curve's slope (rS = -0.46; p = 0.04) and plateau (rS = 0.45; p = 0.04). Discussion: Overall, this study showed that pain-induced CSE changes were associated with changes in muscle coordination, with participants exhibiting greater CSE changes also showing greater coordination changes.
BACKGROUND:Myasthenia Gravis (MG) is a rare autoimmune disorder with fluctuating weakness and substantial impact on quality of life (QoL). Despite advances in pharmacological treatment, patients often experience fatigue, anxiety, and reduced daily functioning. Adapted Physical Activity (APA) has shown benefits in chronic neuromuscular disorders, while Art Therapy (AT) has demonstrated positive psychosocial effects in neurological conditions. However, no studies have investigated the potential synergy of APA combined with AT in MG. METHODS:We designed a monocentric, prospective, randomized crossover pilot trial to evaluate the feasibility and preliminary efficacy of an integrated APA + AT program compared to APA alone. A total of 102 adult patients with MG will be recruited from Lille University Hospital and partner centers. Each participant will undergo two 6-week phases (APA only vs APA + AT), separated by a 46-week washout. Primary outcome is change in QoL (MG-QOL15) at 3 months. Secondary outcomes include fatigue (FSS), anxiety and depression (HADS), activities of daily living (MG-ADL), physical function tests, physical activity (IPAQ, accelerometry), and psychosocial outcomes assessed through qualitative methods (interviews, ethnography, creative elicitation). Quantitative data will be analyzed with repeated-measures models; qualitative data will undergo thematic analysis. DISCUSSION:This trial will be the first to explore a combined APA + AT intervention in MG. By addressing both physical and psychosocial dimensions, the study may provide evidence for integrated, patient-centered care strategies in rare neuromuscular disorders. If feasible and effective, results could inform future multicenter trials and clinical practice. TRIAL REGISTRATION:ClinicalTrials.gov Identifier: NCT07125105.
A pointing task in healthy individuals subjected to experimental pain shed light on the impact of kinesiophobia on pain-induced motor changes. People experiencing kinesiophobia are more likely to develop persistent disabilities and chronic pain. However, the impact of kinesiophobia on the motor system remains poorly understood. We investigated whether kinesiophobia could modulate shoulder pain-induced changes in (1) kinematic parameters and muscle activation during functional movement and (2) corticospinal excitability. Thirty healthy, pain-free subjects took part in the study. Shoulder, elbow, and finger kinematics, as well as electromyographic activity of the upper trapezius and anterior deltoid muscles, were recorded while subjects performed a pointing task before and during pain induced by capsaicin at the shoulder. Anterior deltoid cortical changes in excitability were assessed through the slope of transcranial magnetic stimulation input-output curves obtained before and during pain. Results revealed that pain reduced shoulder electromyographic activity and had a variable effect on finger kinematics, with individuals with higher kinesiophobia showing greater reduction in finger target traveled distance. Kinesiophobia scores were also correlated with the changes in deltoid corticospinal excitability, suggesting that the latter can influence motor activity as soon as the motor signal emerges. Taken together, these results suggest that pain and kinesiophobia interact with motor control adaptation.
BACKGROUND:The Fear-Avoidance Components Scale (FACS) is a reliable and valid instrument widely used to assess fear-avoidance beliefs related to pain and disability. However, there is a scarcity of validated translations of the FACS in different cultural and linguistic contexts, including the French population. This study aimed to translate and validate the French version of the FACS (FACS-Fr/CF), examining its psychometric properties among French-speaking individuals.METHODS:A cross-cultural translation process-including forward translation, backward translation, expert committee review, and pre-testing-was conducted to develop the FACS-Fr/CF. The translated version was administered to a sample of French-speaking adults (n = 55) with chronic musculoskeletal pain. Internal consistency (including confirmatory analyses of the 2 factors identified in the Serbian version), test-retest reliability and convergent validity were then assessed.RESULTS:The FACS-Fr/CF demonstrated high global internal consistency (α = 0.94, 95% CI: 0.91-0.96) as well as high internal consistency of the 2 factors identified in the Serbian version (α = 0.90, 95% CI: 0.86-0.94 and α = 0.90, 95% CI: 0.85-0.94, respectively). Test-retest analysis revealed a moderate (close to high) reliability (ICC = 0.89; 95% CI: 0.82-0.94 and r = 0.89; p<0.005). Convergent validity was supported by significant correlations between the FACS-Fr/CF scores and the Tampa Scale for Kinesiophobia (r = 0.82; p < 0.005), the Pain Catastrophizing Scale (r = 0.72; p < 0.005) and the Hospital Anxiety and Depression Scale (r = 0.66; p < 0.005).CONCLUSION:The present study provides evidence for the cross-cultural translation and psychometric validation of the FACS-Fr/CF. The FACS-Fr/CF exhibits a high internal consistency, a moderate (close to high) test-retest reliability, and good construct validity, suggesting its utility in assessing fear-avoidance beliefs in the French-speaking population. This validated tool can enhance the assessment and understanding of fear-avoidance behaviors and facilitate cross-cultural research in pain-related studies.
In writer's cramp (WC), a form of focal hand dystonia, cortical GABAergic inhibitory mechanisms are altered and may cause involuntary tonic contractions while writing. The objective of this study was to explore the time course of long‐interval intracortical inhibition (LICI) that involves gamma‐amino butyric acid (GABA)‐B transmission and late cortical disinhibition (LCD) (that combines GABA‐A and GABA‐B mechanisms) in patients with WC and in control subjects. A double pulse transcranial magnetic stimulation protocol was used to evoke LICI and LCD while the subjects either gripped a cylinder between their thumb and index fingers or relaxed all their upper limb muscles. We measured the ratio between primed and unprimed motor evoked potential in the first dorsal interosseous at interstimulus intervals ranging between 60 and 300 ms. Though the cortical silent period was not different between the groups, LICI lasted longer in patients with WC, that is, LCD was delayed for more than 30 ms and reached a higher level. In addition to the alteration of inhibitory mechanism mediated by GABA‐B transmission, LCD which probably involves presynaptic inhibition is also modified in patients with WC with possible consequences on the activity of primary motor cortex inhibitory and excitatory circuits which control the hand muscles.caus
The posterior parietal cortex (PPC) is a key structure for visual attention and upper limb function, two features that could be impaired after stroke, and could be implied in their recovery. If it is well established that stroke is responsible for intra- and interhemispheric connectivity troubles, little is known about those existing for the contralesional PPC. In this study, we aimed at mapping the functional (using resting state fMRI) and structural (using diffusion tensor imagery) networks from 3 subparts of the PPC of the contralesional hemisphere (the anterior intraparietal sulcus), the posterior intraparietal sulcus and the superior parieto-occipital cortex to bilateral frontal areas and ipsilesional homologous PPC parts in 11 chronic stroke patients compared to 13 healthy controls. We also aimed at assessing the relationship between connectivity and the severity of visuospatial and motor deficiencies. We showed that interhemispheric functional and structural connectivity between PPCs was altered in stroke patients compared to controls, without any specificity among seeds. Alterations of parieto-frontal intra- and interhemispheric connectivity were less observed. Neglect severity was associated with several alterations in intra- and interhemispheric connectivity, whereas we did not find any behavioral/connectivity correlations for motor deficiency. The results of this exploratory study shed a new light on the influence of the contralesional PPC in post-stroke patients, they have to be confirmed and refined in further larger studies.
Dans la crampe de l’écrivain, une forme de dystonie focale de fonction, certains mécanismes inhibiteurs GABAergiques corticaux comme l’inhibition corticale à courte latence (SICI) sont altérés et pourraient être à l’origine de contractions toniques involontaires au cours du mouvement. D’autres mécanismes GABAergiques ont été mis en évidence chez l’homme, l’un mettant en jeu des récepteurs GABA-B, l’inhibition intracorticale à longue latence (LICI), l’autre, la désinhibition corticale à longue latence (LCD) associant les deux mécanismes GABA-A et GABA-B. Seules deux études ont exploré la LICI chez des patients atteints de crampe de l’écrivain, avec des résultats contradictoires. La LCD n’a quant à elle jamais été explorée chez ces patients. L’objectif de cette étude était d’étudier le décours de la LICI et de la LCD chez des patients atteints de la crampe de l’écrivain et des sujets contrôles. Un protocole de doubles chocs TMS a été utilisé : un premier choc supraliminaire était délivré en regard de la zone du cortex moteur primaire contrôlant le muscle premier intersosseus dorsalis, suivi à des intervalles compris entre 50ms et 300ms d’un second choc supraliminaire alors que les sujets réalisaient une tâche de pince de précision entre le pouce et l’index. Nos résultats montrent que la LICI était prolongée chez les patients dystoniques et que la LCD intervenait à des intervalles interstimuli plus longs et de manière plus marquée. Ces résultats suggèrent que les mécanismes GABA-B sont également altérés dans la crampe de l’écrivain et pourraient contribuer aux déficits sensorimoteurs.
La cocontraction spastique est fréquemment rencontrée chez les patients post-AVC mais l’influence de la fatigue musculaire sur ces cocontractions est mal connue. Évaluer l’effet induit par un protocole isocinétique de fatigue du quadriceps sur le degré de cocontraction entre extenseurs de genou (droit antérieur, vastes latéral et médial) et ischio-jambiers (semi-tendineux) durant la flexion de genou chez des patients hémiparétiques post-AVC chroniques. Secondairement, évaluer l’effet de ce protocole sur le degré de spasticité du quadriceps, sur les paramètres spatio-temporels et de l’endurance à la marche. Étude exploratoire prospective monocentrique de 27 patients hémiparétiques présentant un stiff knee gait. Protocole de fatigue côté hémiparétique : alternance d’extensions actives concentriques maximales de genou avec retours passifs en flexion jusqu’à fatigue musculaire effective. Paramètres mesurés avant/après protocole : indice EMG de cocontraction (ICC) entre droit antérieur, vastes latéral et médial versus semi-tendineux, indice de recrutement agoniste du semi-tendineux (IRA), spasticité (Tardieu), pic de couple de flexion et extension de genou, paramètres spatio-temporels (Gaitrite), vitesse maximale (10MWT), endurance et effort perçu à la marche. Après fatigue, diminution significative du pic de couple isométrique du quadriceps (p = 0,014) sans modification majeure de l’ICC et de l’IRA. Amélioration significative de la spasticité du quadriceps, du 10MWT, de l’endurance et des paramètres spatio-temporels de marche (vitesse, cadence et longueur du pas côté parétique). Effet positif d’un protocole isocinétique de fatigue du quadriceps sur plusieurs paramètres de marche dont la vitesse, sans effet sur les cocontractions spastiqueschez des patients hémiparétiques chroniques post-AVC.
Impaired locomotion is a frequent and major source of disability in patients with neurological conditions. Different neuroimaging methods have been used to understand the brain substrates of locomotion in various neurological diseases (mainly in Parkinson's disease) during actual walking, and while resting (using mental imagery of gait, or brain-behavior correlation analyses). These studies, using structural (i.e., MRI) or functional (i.e., functional MRI or functional near infra-red spectroscopy) brain imaging, electrophysiology (i.e., EEG), non-invasive brain stimulation (i.e., transcranial magnetic stimulation, or transcranial direct current stimulation) or molecular imaging methods (i.e., PET, or SPECT) reveal extended brain networks involving both grey and white matters in key cortical (i.e., prefrontal cortex) and subcortical (basal ganglia and cerebellum) regions associated with locomotion. However, the specific roles of the various pathophysiological mechanisms encountered in each neurological condition on the phenotype of gait disorders still remains unclear. After reviewing the results of individual brain imaging techniques across the common neurological conditions, such as Parkinson's disease, dementia, stroke, or multiple sclerosis, we will discuss how the development of new imaging techniques and computational analyses that integrate multivariate correlations in "large enough datasets" might help to understand how individual pathophysiological mechanisms express clinically as an abnormal gait. Finally, we will explore how these new analytic methods could drive our rehabilitative strategies.
Parietofrontal (PF) networks link the posterior parietal cortex to premotor and prefrontal areas, and are involved in the control of many motor and cognitive behaviors in healthy humans. In recent years, electrophysiological experiments have provided a better understanding of the functional specificity and temporal involvement of the PF networks’ different components during the planning of visually guided upper limb movements. In particular, transcranial magnetic stimulation has been used to temporarily inactivate a cortical area (virtual lesions) or to assess connectivity using paired-pulse protocols)). This approach has shed new light on the neural mechanisms that underlie the planning stages of the reaching and grasping phases of transitive movements. Reaching and grasping were often presented as two distinct processes; in fact, the respective involvement of dorsolateral and dorsomedial networks may depend on the movement's complexity and the need for precise coordination between the two phases. The dorsolateral parietofrontal network (linking the anterior part of the intraparietal sulcus to the ventral premotor cortex) is involved in the grasping phase (i.e. hand shape and grip force scaling), whereas the dorsomedial part (from the posterior part of the intraparietal sulcus and the superior parieto-occipital cortex to the dorsal premotor cortex) appears to be involved not only in the reaching phase but also in more complex visually guided grasping movements. Changes in parietofrontal connectivity following brain injury might explain the impairments in visually guided upper limb movements observed in patients (such as optic ataxia and the motor component of spatial neglect). Lastly, parietofrontal changes may reflect neuronal plasticity in motor function recovery.