Rozprawy doktorskie na temat „Muscle rigidity”

Rigidity is one of the cardinal symptoms in Parkinson's disease, along with Bradykinesia, tremor and postural instability. Rigidity in PD has been understudied, but its pathophysiological basis remains unclear. Various types of neurophysiological and biomechanical approach have been developed in order to investigate the neural control of muscle tone. A common approach is to observe the sensitivity of muscle resistance in response to stretch velocity or displacement [Kamper, Rea, He]. A recent study on elbow flexors in patients with spasticity and rigidity showed a velocity dependent increase in reactive torque in both groups [Lee H, et al). Even though this Study shows a correlation between elbow flexors and velocity, it doesn't discuss the role of elbow extensors. We studied the rigidity response in the elbow of both arms to different speed movements in 12 patients suffering from Parkinson's disease ON or OFF medication. The purpose of this study was to look at both elbow flexion and extension and show that quantitative measures of rigidity and movement disorders in subjects with Parkinson's disease correlate with the currently used clinical evaluations and also find the correlation between velocity and both elbow extension and flexion at the same time. Elbow was flexed and extended by means of a robotic arm,under four different speeds. The resistance to movement was recorded with a torque sensor and EMG of two elbow muscles; Biceps and Triceps; was recorded while the subjects were attempting to relax. The patients were also examined by physicians and their elbow rigidity and muscle tone and Parkinson's disease stage was evaluated and a Universal score in the categories of UPDRS, MMSE, and CAPIT was assigned for each arm of each individual. In the end we will argue that there is a very strong correlation between speed and elbow Extension and Flexion, muscle activity and the rigidity presented in each arm. We will also present the correlation between the robotic torque measurement and the clinical scores given to each subject.

This study focuses on developing a new approach to seated work positions. It was conducted on 67 office workers who use the Video Display Terminal (VDT) as a major function of their working day. Muscle tension was measured by surface electromyography when subjects were asked to adopt four selected working postures. Pain was measured before and after ergonomic intervention on the Nordic scale, which was modified for this study. Performance was measured on timed typing tests. A psychosocial questionnaire was used to determine influences of job demands, and a diagnostic assessment was performed to determine symptoms and pre-existing musculoskeletal conditions. Furniture was used to place subjects in desired positions during the clinical testing sessions and the extended intervention period. The chair seat pan was adjusted to a forward tilt to promote a lordotic curve of the low back, resulting in an erect upper body and upright head position. The desk and keyboard were adjusted to the proper height for each worker. A neutral wrist position was obtained by lowering and tilting the keyboard away from the user. Results revealed muscle tension scores in the upper trapezius and forearm extensors were significantly reduced when the workers were placed with the head in a midline position, with forward-tilting seating and with use of a negative sloping keyboard tray. Subjects reported low pain scores at pretest so no changes were noted after intervention. Loss of control over job elements, lack of job satisfaction, and fear of job loss were related to an increase in muscle tension. Only fear of job loss correlated to increased pain levels. There was no relationship between any of the job demand factors and performance.

Background: Spasticity is a common neurological impairment after injury to the central nervous system, but the neural and biomechanical contributions to it are still poorly understood. Histopathological studies have demonstrated a generalized increase in extracellular connective tissue in spastic muscles, which can decrease its compliance, and reduce the threshold for stimulation of the spindle receptors. Here we propose and provide preliminary evidence for a novel hypothesis for exacerbation of spasticity in an immobilized limb - the hyaluronan hypothesis. We hypothesize that the extracellular connective tissue, which is composed chiefly of hyaluronan, becomes hyper-viscous and stiff in an immobilized limb due to its non-Newtonian properties. Methods: In this case series, we assessed the safety, tolerability, and efficacy of human recombinant hyaluronidase, which hydrolyzes hyaluronan, in combination with saline in restoring tissue compliance. Twenty-one individuals, with moderate-severe upper limb spasticity affecting more than one joint, received multiple intramuscular injections of hyaluronidase-saline. Adverse effects were monitored over 15 weeks. The Modified Ashworth Scale (MAS) assessed reduction in spasticity while active and passive range of motion was assessed using quantitative video analysis of upper limb movement. Findings: 21 participants were included. The procedure was well tolerated. Extensive safety monitoring in all patients revealed no clinically significant adverse events at 15 weeks. Treatment seemed to be effective at reducing spasticity in all twenty-one participants who received the injections (p<0.05 in 16 evaluation over 24 in passive ROM and 17 over 24 in active ROM). The measures of motor function (MAS) showed still improvement at 15 months (p=.000). Interpretations: Subcutaneous administration of hyaluronidase-saline in a multiple sites was fairly safe and well tolerated in adult patients with spasticity; however, these results must be viewed as preliminary until data from blinded, controlled clinical trials are available.
Introduzione: La spasticità è un danno neurologico comune conseguente ad una lesione al sistema nervoso centrale, ma i contributi neurali e biomeccanici ad esso correlati sono ancora poco conosciuta. Studi istopatologici hanno dimostrato un aumento generalizzato nel tessuto connettivo extracellulare nei muscoli spastici, che può diminuire la sua funzionalità e ridurre la soglia per la stimolazione dei fusi neuromuscolari. Con questo lavoro proponiamo e forniamo le prove preliminari per una nuova ipotesi per l'esacerbazione della spasticità in un arto immobilizzato: l'ipotesi ialuronato. Si Ipotizza che il tessuto connettivo extracellulare, che è composto principalmente da ialuronato, diventi iper-viscoso e rigido in un arto immobilizzato grazie alle sue proprietà non-Newtoniane. Metodi: In questo case series, è stata valutata la sicurezza, tollerabilità e efficacia della ialuronidasi ricombinante umana, che idrolizza lo ialuronato, in combinazione con una soluzione salina per ripristinare la funzionalità dei tessuti. Ventuno persone fisiche, con moderata-grave spasticità degli arti superiori in più di una articolazione, hanno ricevuto multiple iniezioni intramuscolari di ialuronidasi-salina. Gli effetti avversi sono stati monitorati per 15 settimane. La Modified Ashworth Scale (MAS) ha valutato la riduzione della spasticità mentre la l’escursione articolare di movimento attiva e passiva è stata valutata mediante analisi quantitativa del movimento dell'arto (ROM) superiore tramite video. Risultati: 21 partecipanti sono stati inclusi. La procedura è stata ben tollerata. Il monitoraggio estensivo sulla sicurezza dei pazienti non ha rivelato eventi avversi clinicamente significativi a 15 settimane. Il trattamento è risultato efficace nel ridurre la spasticità in tutti i ventuno partecipanti che hanno ricevuto le iniezioni (p <0.05 di 16 valutazione su 24 nella ROM passivo e 17 su 24 nel ROM attivo). Le misure di funzione motoria (MAS) hanno mostrato un mantenimento del miglioramento a 15 mesi (p = 0,000). Conclusioni: La somministrazione di ialuronidasi-salina in più siti è risultata sicura e ben tollerata in pazienti adulti con spasticità; tuttavia, questi risultati devono essere visti come preliminari fino a quando ulteriori studi clinici controllati in cieco non saranno disponibili.

La matrice extracellulaire (MEC) subit plusieurs modifications au cours du vieillissement, ce qui altère ses propriétés biomécaniques. Les cellules responsables de la régénération de la portion myogénique du muscle sont les cellules satellites, qui, une fois activées, sont appelées les cellules progénitrices myogéniques (CPM). La rigidité du muscle, influence le devenir des CPM. La capacité régénérative du muscle squelettique diminue lors du vieillissement. Nous avons posé l’hypothèse selon laquelle la rigidité observée dans le tissu âgé pourrait nuire à la capacité régénérative des CPM. Nous avons tout d’abord validé les modifications subies par la MEC suite au vieillissement en les comparant au tissu adulte. Les résultats montrent une augmentation de la quantité de collagènes et de réticulation non enzymatique. En plus, une augmentation de la rigidité du muscle et des fibres individualisées a été observée par microscopie à force atomique (AFM). L’équipe s’est ensuite intéressée à leur activité myogénique dans un modèle de fibres musculaires en culture (ex vivo). Nous avons observé une diminution du nombre de cellules myogéniques sur les fibres de tissus âgés, comparativement aux tissus adultes. Nous avons montré que les proportions de cellules quiescentes sont plus élevées sur des fibres adultes suite à l’isolement et que les proportions de cellules prolifératives et en voie de différenciation sont plus élevées sur les fibres âgées. De plus, sur des fibres endommagées gardées en culture six jours, nous avons observé que les proportions de cellules prolifératives sont plus élevées sur les fibres adultes et que celles des cellules en voie de différenciation sont plus élevées sur les fibres âgées. Enfin, nous avons observé l’activité myogénique des CPM ainsi que l’impact de la rigidité en culture (in vitro). Nous n’avons observé aucune différence des capacités de prolifération et de différenciation des myoblastes adultes et âgés. En terminant, nos recherches ont montré qu’une rigidité de 2.0 kPa favorise un état prolifératif tandis qu’une rigidité de 18 kPa stimule plutôt l’engagement vers la différenciation. Ces résultats suggèrent que la rigidité peut être une cause de la diminution du potentiel régénératif du muscle vieillissant. En résumé, ces travaux soulignent l’importance de l’augmentation de la rigidité du microenvironnement sur les CPM comme cause de la diminution du potentiel de régénération du muscle vieillissant.

La rigidité artérielle et la fibrose ont une valeur prédictive dans le développement des maladies cardiovasculaires (CV). Ces 2 phénotypes impliquent les cellules musculaires lisses vasculaires (CMLVs) notamment des récepteurs membranaires et les protéines du cytosquelette. Les objectifs ont été d’étudier : (i) l’influence du récepteur minéralocorticoïde (MR) sur la réactivité vasculaire, (ii) le rôle de l’intégrine αvβ3 dans le développement de la rigidité artérielle et la fibrose vasculaire, et (iii) l’impact de la vimentine et la synémine sur la structure et la fonction artérielle. Ces trois études ont utilisées des souris avec invalidation génétiques des protéines d’intérêt. Résultats : l’absence du MR diminue la réactivité vasculaire en altérant le couplage contraction/relaxation des CMLVs via des mécanismes Ca2+- et NO-dépendants (une diminution de la vasoconstriction en réponse au Ca2+ extracellulaire et une altération de la vasorelaxation endothélium-dépendante en réponse à l’acétylcholine). L’invalidation de la sous-unité αv prévient la fibrose en réponse à l’administration d’angiotensine II. L’absence de la vimentine et non celle de la synémine augmente la rigidité artérielle via des changements des adhésions focales des CMLVs mais aussi des cellules endothéliales. En conclusion, les récepteurs membranaires et protéines intracellulaires étudiées influencent la fonction et la structure des artères grâce à des actions spécifiques sur le tonus musculaire, la mécanotransduction et l’organisation ultra-structurale des CMLVs. Ces études montrent au niveau cellulaire et moléculaire le déterminisme plurifactoriel des phénotypes de rigidité-fibrose de la paroi artérielle. Ces résultats nécessitent des travaux plus mécanistiques pour affirmer l’implication de ces protéines dans les maladies CV liées au vieillissement
Arterial stiffness and fibrosis have a predictive value in the development of cardiovascular diseases (CV). These two phenotypes involve vascular smooth muscle cells (VSMCs) including membrane receptors and cytoskeletal proteins. The objectives were to examine: (i) the influence of the mineralocorticoid receptor (MR) on vascular reactivity, (ii) the role of avb3 integrin in the development of arterial stiffness and vascular fibrosis, and (iii) the impact of vimentin and synemin on arterial structure and function. The mice with genetic invalidation of the proteins of interest were used in these three studies. Results: the absence of MR decreased vascular reactivity by altering the contraction/relaxation coupling of VSMC through Ca2+- and NO-dependent mechanisms (a decrease of vasoconstriction in response to extracellular Ca2+ and impaired endothelium-dependent vasorelaxation in response to acetylcholine). The invalidation of the αv subunit prevented fibrosis in response to the administration of angiotensin II. The absence of vimentin, and not that of the synemin, increased arterial stiffness via changes in focal adhesions of VSMCs as well as endothelial cells. In conclusion, the studied membrane receptors and intracellular proteins that influenced the structure and function of arteries through specific actions on muscle tone, the mechanotransduction and the ultra-structural organization of VSMCs. These studies show the multifactorial dependency of the stiffness-fibrosis phenotypes of the arterial wall at the cellular and molecular levels. These results require more mechanistic work to determine the role of these proteins in CV diseases related to aging

La methodologie developpee au cours de ce travail permet la modelisation du comportement de la rigidite face a la contrainte d'un muscle papillaire (isole de cur de rat) a un moment determine de son activation. Appliquee a differents instants de l'activite du muscle stimule, cette methodologie rend compte de l'evolution de la relation rigidite-contrainte en fonction du degre d'activation. La meme procedure est appliquee au muscle papillaire de cur hypertrophie (hypertrophie induite par hypertension renovasculaire: modele 2k-1c rhr). Les resultats obtenus montrent que dans certaines conditions de fonctionnement, la resistance opposee par le muscle a une augmentation de la contrainte fait intervenir a la fois une resistance elastique et une resistance visqueuse. L'expression de la resistance visqueuse depend de la vitesse de variation de la contrainte et semble en outre controlee par les phenomenes activateurs de la force musculaire au niveau cellulaire. La rigidite apparait donc comme un phenomene viscoelastique dont l'intensite est modulable par les processus actifs de la contraction au travers de proprietes encore peu connues de la viscosite musculaire. La resistance a la contrainte determinee en relaxation subit un accroissement significatif au cours de l'hypertrophie. Cette anomalie semble etre liee directement aux perturbations des mouvements du calcium dans le myocyte pathologique. Ainsi, dans le cur, tout agent pharmacologique ou tout mecanisme pathologique ayant une incidence sur le metabolisme du calcium pourrait avoir des consequences notables sur la rigidite par modification de la resistance visqueuse

La myopathie myofibrillaire est une maladie neuromusculaire à évolution lente caractérisée par de graves troubles musculaires causés par des mutations dans le gène codant pour des protéines du cytosquelette. L'un des gènes affectés en relation avec le développement de la MFM est DES. Des mutations dans le gène de la desmine entraînent des myopathies des muscles squelettiques et cardiaques. Cependant, les évènements qu'elles entraînent et qui sont à l’origine des phénotypes pathologiques cardiaques restent mal connus. Mon objectif est de créer un modèle in vitro de MFM basé sur des cellules souches pluripotentes humaines afin d'étudier le rôle des mutations spécifiques dans la desmine sur le développement et la fonction des cellules cardiaques. Pour atteindre cet objectif, en collaboration avec les docteurs A. Behin, K. Wahbi et la société Phenocell, nous avons généré des iPSC à partir des cellules sanguines périphériques de patients souffrant d'une forme de cardiomyopathie induite par une mutation de la desmine. Les lignées iPSC générées contenant les mutations du gène codant la desmine ont permis d’étudier le rôle d’une mutation dans la spécification et la fonction des cardiomyocytes. La bioénergétique mitochondriale, la structure cellulaire et la fonction contractiles ont été évaluées au niveau cellulaire. En conclusion, il convient de noter que les mutations de la desmine conduisent à une désorganisation des structures des sarcomères dans les cardiomyocytes et à une perturbation de l'expression des protéines mitochondriales. Ce qui conduit à une altération des fonctions de la mitochondrie. Ces données permettent d’améliorer notre compréhension des mécanismes moléculaire qui sous-tendent le développement de la MFM
Myofibrillar Myopathy is a slowly progressive neuromuscular disease characterized by severe muscular disorders caused by mutations in the gene encoded cytoskeletal proteins. One of the genes described in connection with the development of MFM is DES. Mutations in the desmin gene lead to skeletal and cardiac muscles myopathies. However, the cardiac pathological consequences caused by them remain poorly understood. My objective is to create an in vitro human stem cell model of MFM to specifically investigate the role of patient-specific mutations in desmin on cardiac lineage development and function. To achieve that objective, in collaboration with Drs. Behin and K. Wahbi and Phenocell, we generate patient-specific iPSC from peripheral blood cells of the patient suffering severel form of desmin-deficient cardiomyopathy. The generated iPSC lines carrying DES gene mutations enable a powerful examination of the role of desmin mutation on cardiomyocyte specification and function. Bioenergetic, structural, and contractile function will be assessed in a single cell. In conclusion, it should be noted that desmin mutations lead to a disorganization of sarcomere structures in cardiomyocytes and to a perturbation of mitochondrial protein expression. This leads to a distortion of functions in the mitochondria. These data facilitate the understanding of the molecular pathway underlying the development of desmin-related myopathy. And the system we have created could also allow us to better evaluate the correlation between the desmin genotype and phenotype in terms of effect on the heart

Nous avons étudié les adaptations fonctionnelles de divers muscles squelettiques, sous l'effet d'un entraînement à l'exercice de haute intensité: le saut en hauteur. L'analyse mécanique révèle un accroissement des résistances et raideurs passives des muscles pennés Extensor Digitorum Longus (EDL) et Rectus Femoris (RF) à l'issue de l'entraînement, en sus de l'augmentation générale induite par l'âge. Cet accroissement des qualités mécaniques passives semble associé à une augmentation de la concentration en collagène au niveau des muscles. L'élévation du taux de collagène, particulièrement sous sa forme non-soluble est une constante avec l'âge, qui peut être en partie attribuée à une baisse du processus de dégradation. Néanmoins, la présence de concentration accrue en collagène dans les muscles des lapins entraînés, semble être imputable à un niveau supérieur de synthèse du collagène de type I. En effet, nous avons montré que l'exercice induisait le maintien d'un taux d'ARNm du procollagène a1(I) très supérieur dans les muscles de lapins entraînés, alors que ce même taux baisse conséquemment avec l'âge chez les animaux sédentaires. .
The functional adaptations of various skeletal muscles, were investigated in response to a high-intensity exercise training, i. E. Jumping. The mechanical analysis reveals an increase in resistance and passive stiffness of pennate Extensor Digitorum Longus (EDL) and Rectus Femoris (RF) muscles after training, in addition to a general increase induced by age. This increase in passive mechanical qualities could be linked to an increase in collagen concentration of muscles. .

Thesis (M.A.)--Sam Houston State University, 2005.
Includes bibliographical references (leaves 38-44). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Dissertation submitted in fulfillment of requirements for a Master's Degree in Technology: Chiropractic, Durban University of Technology, 2007.
Delayed onset muscle soreness (DOMS) is muscular pain which ranges from mild discomfort to severe debilitating pain, caused by eccentric exercise. It generally sets in 12 - 24 hours after the causative activity and subsides within approximately seven days. The aim of this study was to determine whether proprioceptive neuromuscular facilitated (PNF) stretching immediately after eccentric exercise was more beneficial than PNF stretching 24 hours after eccentric exercise on the muscle pain experienced in DOMS. This study was a prospective, randomised clinical trial. Thirty healthy sedentary male participants were randomly selected to participate in the study by advertising in local newspapers and pamphlet distribution in Durban and its surrounding areas. The patients' ages ranged from 20 to 32 years of age. Subjective and objective readings were taken at the beginning and end of each visit, over the three-day study period. This was done with the numerical pain rating scale and the algometer force gauge, respectively. Baseline measurements were taken before any exercise or stretching at the initial visit. All participants then were asked to do squats until fatigue to induce delayed onset muscle soreness. III The participants were divided randomly into two groups, Group A and Group B. The former group underwent PNF stretching immediately after exercise and the latter group underwent PNF stretching twenty four hours after exercise. Both groups were asked to return for two subsequent days following the initial visit and they again underwent PNF stretching at each visit. Comparison was made between the individual patients' pain perception over time, as well as between each group. Descriptive analysis was done using frequency tables (reporting counts and percentages) for categorical variables and summary statistics (reporting mean, standard deviation and range), for quantitative variables. Baseline and demographic characteristics were compared between the two treatment groups using independent t-tests for quantitative variables and Pearson's chisquare tests for categorical variables. The treatment effect was assessed using repeated measures ANOVA testing. Statistical analysis revealed that there was no difference in the improvement of pain experienced between the two groups. However, Group B (PNF stretching 24 hours after exercise) appeared to improve at a greater rate than Group A (PNF stretching immediately after exercise). A larger study needs to be conducted in order to provide statistically relevant results.
M

Dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Chiropractic, Durban University of Technology, 2009.
Through the literature review it has become apparent that low back pain is a very real problem in most societies. It has been suggested that there is enough evidence to prove the relationship between low back pain and local muscle dysfunction and that focus in management of these patients should be the rehabilitation of these muscles by exercise. Literature suggests that optimal core muscle strength, control and endurance working synergistically with the rest of the neuromusculoskeletal system is necessary for lumbar spine stability . Arthrogenic Muscle Inhibition is caused by distension and/or damage of a joint and is thought to disable the muscle from contracting all its muscle fibres. When a joint is injured it is thought that AMI causes muscle weakness, which in turn hampers the rehabilitation process of that joint despite complete muscle integrity. Spinal manipulative therapy has been shown to alter the excitability of spinal muscle motor neurons due to the stimulation of mechanoreceptors in the joint capsules suggesting that SMT could be a means to remove this inhibitory action. The literature supports the hypothesis that a decrease in the neurological deficit caused by AMI may result in a faster recovery rate. Aims The aim of this study is to determine the immediate effect of thoraco-lumbar spinal manipulation compared to lower lumbar spinal manipulation on core muscle endurance and activity in patients with mechanical low back pain by assessing the correlation between the objective and subjective measures. Method A prospective, convenience sample with purpose allocation (pre /post) clinical trial was used as the sampling method. Thirty participants where placed in two groups, group one and group two, of fifteen people each. Group one underwent spinal v manipulative therapy between L4 and S1 spinal levels. Group two underwent spinal manipulative therapy in between T8 and L1 spinal levels. The objective and subjective testing was done pre- and post-intervention. The objective data was that of a surface EMG attached bilaterally over the internal oblique as well as a prone abdominal draw in biofeedback test. The subjective data included a pain numerical rating scale (0-100). Results The results showed to partially favour group two (thoraco-lumbar), in both increased endurance time that would prove that AMI does in fact inhibit the transversus abdominis and obliques internus, thus it would hinder the rehabilitative process. Some of the statistics where not in favour of the aims, as there was no difference in the effect of group one or two on the NRS, as both improved consistently. It would be recommended that use be made of fine-wire EMG for testing the activity in both the obliques internus and the transversus abdominis, which would allow for more consistent readings, thus adding strength to the research.

Thesis (M.Tech.: Chiropractic)-Dept. of Chiropractic, Durban University of Technology, 2007 xi, 60 leaves, Annexures 1-9
The Transversus Abdominis (TrA) muscle is recognised in the literature as playing a vital and protective role in maintaining a healthy core and aiding lumbar biomechanics in the dampening of external forces applied to the lumbar spine. Pilates purports to employ the principles of core training yet there remains a deficit in the literature despite its popularity in rehabilitation and fitness industries. This study aimed to evaluate the efficacy of Pilates method in training the TrA in comparison to a moderately active population that regularly exercises in a gym environment, as well as a sedentary control.