Rozprawy doktorskie: „Motor periphery”

1

Zapletal, Ladislav. "Řídicí systém kamerového sceneru pro monitorování růstu rostlin". Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2017. http://www.nusl.cz/ntk/nusl-318195.

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This diploma thesis deals with the design and realization of robotic drive of the camera scanner system of plants together with the control unit. This device serves as the carrier system of various camera sensors. The sensors will monitor both the growth and the physiological status of the cultivated plants in the growth chambers. The thesis describes the choice of electronic and mechanical components from which the device is built. The text describes a design of the PCB that will control the device. Part of the thesis is also a demonstration of the realization of the systém together with the illustration of the real form of the system and its testing.

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2

Eggers, Thomas Elliott. "Chronic Peripheral Nerve Recordings and Motor Recovery with the FINE". Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1516624330839376.

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3

Szlavik, Robert Bruce. "In vivo electrical stimulation of motor nerves". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0032/NQ66239.pdf.

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4

Higashimori, Haruki. "Systemic inductive mechanism of burn-induced peripheral motor and sensory neuropathy /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2004. http://uclibs.org/PID/11984.

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5

Pashalis, Despina. "Central cortical processes or peripheral motor processes differentiate extraverts from introverts /". Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09ARPS/09arpsp2818.pdf.

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6

McDowell, Sally-Ann. "The effects of peripheral vision on motor initiation in Parkinson's disease". Thesis, University of Reading, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296634.

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7

Drew, Alexander Peter. "Genetics of distal hereditary motor neuropathies". Thesis, The University of Sydney, 2012. http://hdl.handle.net/2123/8652.

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The distal hereditary motor neuropathies (dHMN) are a clinically and genetically heterogeneous group of disorders that primarily affect motor neurons, without significant sensory involvement. Using genome wide linkage analysis in a large Australian family (CMT54), a form of dHMN was previously mapped by this laboratory, to a 12.98 Mb interval on chromosome 7q34-q36. The axonal neuropathy seen in this family was classified as dHMN1; with autosomal dominant inheritance, early but variable age of onset, and muscle weakness and wasting affecting the lower limbs. In this project, genetic linkage analysis of the chromosome 7q34-q36 disease interval was carried out in the original family (CMT54) and 20 smaller families from an Australian dHMN cohort. Fine mapping in family CMT54, including unaffected individuals suggested a minimum probable candidate interval of 6.92 Mb, flanked by markers D7S615 and D7S2546 within the 12.98 Mb critical disease interval. Of the additional dHMN families, one (family CMT44) achieved suggestive linkage to the chromosome 7q34-q36 disease locus with a LOD score of 2.02. Mutation screening was carried out in family CMT54 at the chromosome 7q34-q36 locus. The 12.9 Mb disease interval contains 89 annotated protein-coding genes, of which 60 lay within the prioritised 6.92 Mb interval. A combination of methods was used to screen these genes for a putative pathogenic mutation. Functional candidate genes were identified via a literature and database search. The coding exons of 35 prioritised candidate genes were sequenced and no pathogenic mutation was identified. Cytogenetic analysis excluded large scale chromosomal abnormalities. Array based comparative genomic hybridisation of the 7q34-q36 interval in patients did not identify any pathogenic duplications or deletions. Next generation sequencing (NGS) techniques were used to identify sequence variants within the remaining genes within the 7q34-q36 interval and elsewhere in the genome. Two NGS based approaches were applied to mutation screening in family CMT54. Initially, the chromosome 7q34-q36 disease interval was analysed in one affected individual using a custom designed DNA capture microarray and 454 GS FLX (Roche) sequencing. Approximately 80% of patient coding exons were captured, sequenced and no pathogenic mutations were identified. The chromosome 7q34-q36 target captured DNA sample was also re-sequenced along with an additional two affected individuals and one unaffected parent using exome capture and Solexa (Illumina) sequencing. Combined, 99.5% of coding exons were sequenced in the chromosome 7q34-q36 interval and all sequence variants that were identified were excluded from a pathogenic role. Sequence variants identified elsewhere in the exome were also excluded from a pathogenic role. Exome sequencing of dHMN family CMT44 did not identify any putative pathogenic mutation at the chromosome 7q34-q36 locus. The exomes of four affected and one unaffected individuals were sequenced. Exome wide analysis identified a potential digenic inheritance in CMT44 of a previously published MFN2 mutation causing a mild CMT2 phenotype and a second mutation causing a dHMN phenotype. Potential candidate mutations for dHMN were identified in two genes, PCDHGA4 and DNAH11. PCDHGA4, was previously shown to function in the brain and spinal cord, and deletion of PCDHG genes in a mouse model causes a severe neurodegenerative phenotype. The gene mutation causing dHMN that maps to chromosome 7q34-q36 remains to be identified. The disease mutation may lie in a coding region not captured by current exome platforms, a non-coding region, or the mutation may cause disease through an alternate mechanism not detected by the methods employed in this thesis. Future studies should concentrate on transcriptome analysis by next-gen RNA sequencing, which may identify unknown transcripts and exons that map to chromosome 7q34-q36 or highlight sequence variants located in regulatory elements. Identification of new gene mutations is critical to further understanding the biochemical and cellular processes underlying dHMN. Although the causative mutation for dHMN on 7q34-q36 was not identified, a significant proportion of the disease interval has been excluded using a combination of traditional and new technologies. The purpose of this thesis is to identify new gene mutations causing dHMN. The genetic and functional data presented here suggest this will be a difficult task; the genetic heterogeneity complicates genetic analysis and the multiple molecular mechanisms implicated to date make it difficult to pinpoint specific candidate genes. The identification of additional genes and genetic modifiers is necessary to increase our understanding of the disease mechanisms causing dHMN and related neuropathies. This will directly aid in the diagnosis and classification of these neurodegenerative diseases and may lead to new therapeutics and treatment strategies.

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8

Wallquist, Wilhelm. "On laminins and laminin receptors and their role in regeneration and myelination of the peripheral nerve /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-781-9/.

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9

Maskill, David William. "Peripheral and central influences on the electromographic responses of muscle to transcranial magnetic stimulation in man". Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283732.

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10

Banks, Daniel John. "Modelling studies on peripheral nerve neural signal transduction using thin-film microelectrodes". Thesis, University of Surrey, 1994. http://epubs.surrey.ac.uk/842690/.

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Functional electrical stimulation (FES) techniques may be used to restore motor function lost or impaired through spinal cord injury. In order to use these techniques to restore complex tasks such as walking, it is necessary to provide sensory feedback to regulate the output of the FES controller. It has been suggested that multi-microelectrode probes (microprobes) implanted into the peripheral nervous system can be used to detect signals originating from the body's own sensors. These signals could be decoded and used to regulate the output of the FES controller. Prior to the present work, however, microprobes had primary been used to study neural activity in the brain, not peripheral nerves. In the present work, locust peripheral nerve has been used as an animal model for experimental and computer modelling work. The experimental work was directed at discerning the detail of information that can be obtained using microprobes to record from peripheral nerves (ie, the selectivity of the probes). In the computer modelling work, the effects of filtering the recorded signal were studied using an electrical circuit simulator programme (SPICE). Finite element analysis software (ANSYS) was used to model the electrical potential distribution in the nerve trunk, and to determine the effects of the probe substrate on the recorded signal. The results of the experimental work indicated that it may be possible to achieve higher selectivity in recording with microprobes than predicted by some models. It is concluded that future models need to represent the situation in greater detail in order to make more realistic predictions regarding the practical work. This will require further data on the electrical properties of the structures modelled within the nerve trunk. The SPICE modelling work successfully predicted the shape of the neural signals that would be recorded in the practical work. The partial differentiating effect of high pass filtering neural signals was also demonstrated. The results of the finite element modelling work demonstrated that the probe substrate would be expected to amplify signals from fibres directly in front of it, and attenuate signals from fibres behind it. This was shown to be significant for probe substrates with dimensions much smaller than the longitudinal spread of the action potential along the fibre. It was also found that these effects can be influenced by the position of the microprobe substrate relative to other structures within the nerve trunk; not just relative to the fibre. The significance of these results as they relate to mammalian nerve is discussed. Improved experimentation techniques and models are outlined, based on the results of this work. These include the requirement for improved facilities to determine the limits of selectivity in recording from peripheral nerves, and also the inclusion of inhomogeneities in models of the nerve trunk to make more realistic predictions regarding practical work. Finally, the development of active probes is discussed, including requirements for particularly novel circuitry, and the integration of many devices into a system to control FES.

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11

Charlton, Shona. "The effect of prolonged peripheral stimulation on the excitability of human motor cortex /". Title page and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09SB/09sbc481.pdf.

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12

Lee, Stella Joonmyung. "A Critical Period for Functional Motor Recovery After Peripheral Nerve Injury in the Mouse". Thesis, Harvard University, 2014. http://etds.lib.harvard.edu/hms/admin/view/64.

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Repair of peripheral nerve injury often results in poor functional motor recovery. This deficit has previously been attributed to the failure of axons to regenerate into the muscle. However, we have recently reported that following nerve injury in mice, axons have regenerated to the motor end plate in animals with poor recovery. We proposed that following axonal injury, there is a critical period during which the axon must reach the muscle in order to form a functional neuromuscular junction. We have developed a mouse model of prolonged denervation, in which the sciatic nerve is crushed repeatedly every few days, preventing regenerating axons from reaching the muscle. This multiple crush model allows us to vary the period of denervation by modifying the number of crushes. Motor recovery as assessed using the toe-spreading score occurs after 3 or 4 multiple crushes every 7 days (24 or 31 days of denervation) but not after 5 crushes (38 days). Immunostaining for alpha-bungarotoxin and neurofilament confirmed end plate reinnervation. Thus following denervation > 38 days, a motor deficit persists despite end plate reinnervation. Although the mechanism for the deficit requires investigation, these results suggest that functional neuromuscular junction reestablishment more than end plate reinnervation and that there is a time limit for functional synapse reformation.

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13

Nelson, Sandahl Hygeia. "Effects on motor neuron development of altering peripheral targets in embryonic leeches (Hirudo verbana)". Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1473082.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed Feb. 1, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 31-32).

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14

Parsons, Perez Maria Cristina. "HSV vectors for gene delivery to motor neurons following peripheral administration : function of Reg-2". Thesis, University College London (University of London), 2003. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398050.

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15

Miressi, Federica. "Hereditary Peripheral Neuropathies : from Molecular Genetics to a cellular model of hiPSC-derived motor neurons". Thesis, Limoges, 2020. http://aurore.unilim.fr/theses/nxfile/default/56675caf-59b3-4af2-ae86-c5e356784128/blobholder:0/2020LIMO0053.pdf.

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La maladie de Charcot-Marie-Tooth (CMT) est la neuropathie périphérique héréditaire la plus fréquente. Actuellement plus de 80 gènes ont été identifiées comme étant à l’origine des CMT, mais le diagnostic génétique est posé seulement dans 30 à 40% des cas. Cette étude avait deux objectifs principaux : dans un premier temps, nous nous sommes intéressés aux CMT et neuropathies périphériques associées via une approche moléculaire et bioinformatique, pour optimiser leur caractérisation génétique ; dans un second temps, nous avons étudié les mécanismes altérés dans une forme axonale de CMT, par la création d’un modèle cellulaire humain de cellules souches humaines induites à la pluripotence (hiPSc) et leur différenciation en motoneurones (MN). Dans la première partie du projet, nous présentons un nouvel outil bioinformatique, CovCopCan, développé au sein de l’équipe pour détecter les Variations du Nombre de Copies (CNV), à partir des données de NGS. Grâce à CovCopCan, deux nouveaux CNV ont été identifiés et nous discutons leur implication dans deux cas complexes de neuropathie périphérique. Nos travaux ont également permis de mettre en évidence trois variations génétiques chez un patient CMT, soulignant que la CMT peut être une pathologie génétique multilocus. Dans la deuxième partie de ce travail, un modèle cellulaire de MN a été créé pour étudier le gène GDAP1 et son implication dans le CMT2H. Nous avons reprogrammé des fibroblastes dermiques de cinq sujets contrôles et de deux patients CMT, portant deux mutations codon-stop homozygotes sur le gène GDAP1, en cellules souches pluripotentes induites humaines (hiPSC). Nous avons ensuite mis au point un protocole de différenciation pour générer des MN à partir d’hiPSC. Les MN avec la mutation p.Ser194* sur GDAP1 ont été analysés par des tests fonctionnels, morphologiques et d’expression. Nous avons confirmé l’expression neuronale de GDAP1, et nous avons mis en évidence que le stress oxydant et la dysfonction mitochondriale étaient à l’origine de la pathologie dans les MN CMT2H. Nos résultats ont montré que les analyses génétique et fonctionnelle sont essentielles pour la caractérisation complète de la maladie de CMT
Charcot-Marie-Tooth (CMT) disease is the most common hereditary peripheral neuropathy. To date, more than 80 genes have been identified to be involved in CMT, but genetic diagnosis is achieved only in 30-40% of cases. This study presented two main objectives: first, we focused on CMT and associated peripheral neuropathies using molecular and bioinformatic approaches to optimize their genetic characterization ; secondly, we investigated impaired mechanisms in an axonal CMT form, by creating a human cellular model of human induced pluripotency stem cells (hiPSC) and their differentiation into motor neurons (MN).In the first part of the project, we developed a new bioinformatic tool, CovCopCan, to detect Copy Number Variations (CNV), starting from NGS data. Thanks to CovCopCan, two new CNV have been identified and we discuss their involvement in two complex cases of peripheral neuropathy. We also identified three genetic variations in a CMT patient highlighting that CMT can be a multilocus genetic pathology. In the second part of the project, we successfully generated a cellular model of MN for the study of GDAP1 gene and its associated CMT2H form. We reprogrammed dermal fibroblasts of five control subjects and two CMT patients, carrying two different homozygous codon-stop mutations in GDAP1, into human inducedpluripotent stem cells (hiPSC). Then, we established a differentiation protocol to generate MN from hiPSC.MN with the GDAP1 p.Ser194* mutation were analyzed by expression, morphological, and functional tests. We confirmed the neural expression of GDAP1, and we suggested that oxidative stress and mitochondrial impairment could be responsible for the pathological condition in CMT2H MN. Taken together, our results highlighted that both genetic and functional analyses are essential in the complete characterization of CMT disease

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Andersen, Mark Bille. "Psychosocial factors and changes in peripheral vision, muscle tension, and fine motor skills during stress". Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184446.

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A theoretical model of stress and athletic injury is presented. The purpose of the dissertation is to propose a comprehensive framework of the stress-injury relationship that includes cognitive, physiological, attentional, behavioral, intrapersonal, social, and stress history variables. Development of the model grew from a synthesis of the stress-illness, stress-accident, and stress-injury literatures. The model and its resulting hypotheses offer a framework for many avenues of research into the nature of injury and reduction of injury risk. Other advantages of the model are that it addresses possible mechanisms behind the stress-injury relationship and it suggests several specific interventions that may help diminish the likelihood of injury. The model also has the potential to be applied to the investigation of injury and accident occurrence in general. A portion of the model is then tested experimentally. Personality, stress, and coping resource variables are used to predict changes in peripheral vision, general muscle tension, heart rate, state anxiety, and fine motor skill (a hand steadiness task) from baseline to stress condition (a dual-task paradigm with noise as an added stressor). There were significant decreases in peripheral vision and hand steadiness accompanied by significant increases in state anxiety and heart rate from baseline to stress conditions. The only significant predictor variable for peripheral vision changes was negative life events. Subjects with high negative life events ratings had greater peripheral vision deficits during stress than subjects who rated low on negative life events. For increases in state anxiety only the self report of how the subject experienced the stress condition was significant. Subjects who rated the stress condition as stressful had greater state anxiety increases than subjects who rated the stress condition as challenging. The results are discussed in terms of future directions for stress-injury research.

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Wagner, Justin. "Whole Exome Sequencing to Identify Disease-Causing Mutations in Lower Motor Neuron Disease and Peripheral Neuropathy". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34124.

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Lower motor neuron diseases and peripheral neuropathies are two groups of diseases that include multiple rare disorders where many causes are unknown and definitive treatments are unavailable. Understanding the molecular etiology of these genetic diseases provides an opportunity for rapid diagnosis, preconception genetic counseling and, in a subset, direction for the development of future treatment options. The recent introduction of whole exome sequencing (WES) marks a new era in Mendelian genetic disease research as the majority of the coding region of the genome can be sequenced in a timely and cost-effective manner. In this study, WES was used to investigate the molecular etiology of a cohort of 37 patients presenting with lower motor neuron disease or peripheral neuropathy. A molecular diagnosis was determined for seven patients informing the diagnostic utility of WES. Novel phenotypes were found for three genes originally associated with a different disorder. Finally, the foundation has been laid, through the use of functional studies and large scale data-sharing, to identify novel disease-causing genes for lower motor neuron disease and peripheral neuropathy.

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18

Johnson, Lise. "DECODING ELECTRIC FIELDS OF THE NERVOUS SYSTEM: INVESTIGATIONS OF INFORMATION STORAGE AND TRANSFER IN THE CENTRAL AND PERIPHERAL NERVOUS SYSTEM". Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/193574.

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Electrical potentials are the fundamental currency of communication in the nervous system. The advanced executive functions of the prefrontal cortex and the motor commands delivered to the neuromuscular junction, though involved with very different aspects of behavior, both rely on time-varying electrical signals. It is possible to "listen to" the internal communications of the nervous system by measuring the electrical potentials in the extra-cellular space. However, this is only meaningful if there is some way to interpret these signals, which are incredibly complicated and information rich. This dissertation represents an attempt to decode some of these signals in order to reveal their significance for behavior and function. The first study is an investigation of the relationship between different elements of the local field potential in the prefrontal cortex and memory consolidation. It is shown that certain electrographic signatures of non-rapid eye movement sleep, namely K-complexes and low-voltage spindles, are correlated with neuronal replay of recent experiences. It is also shown that the global fluctuations of activity in the population of cells, known as up/down states, is correlated with neuronal replay. Finally, it is shown that high-voltage spindles are not correlated with memory replay, and are therefore functionally different from low-voltage spindles. The second study focuses on the relationship between movements of the upper limb and the coordinated neural control, as measured by the electromyogram (EMG), of the muscles generating that movement. We show that different probability-based models can be used to predict what the pattern of EMG in the different muscles will be for any given kinematic state of the hand. In the third study it is demonstrated that the kinematic output associated with a particular pattern of EMG can be reproduced with electrical stimulation. Thus, it is not only possible to understand the commands issued by the nervous system, it is also possible to issue commands by interfacing with the nervous system directly. Finally, the design for an experiment that would combine EMG prediction with translation of EMG into electrical stimulus patterns is presented. The objective of this study would be to use these methods to fully control the upper limb in a way that would be useful for a functional electrical stimulation-based neuroprosthetic for spinal cord injured patients.

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Van, Dyk A. P. "The effects of a sports vision training programme on selected visual-motor skills in a non-fatigued and fatigued cardiovascular condition". Thesis, University of the Western Cape, 2014. http://hdl.handle.net/11394/4284.

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Philosophiae Doctor - PhD
The aim of the study was to determine the effects of a sports vision training programme on peripheral awareness, eye-hand coordination, eye-body coordination, visual reaction time and visual-motor response time of physically active males when in a non-fatigued condition and when in an induced-fatigue condition that simulates levels experienced when playing field-based sports. Scheduling challenges made it necessary to use a sample of convenience rather than random sampling to divide the 49 participants into a treatment group (n=16) and a control group (n=33). A pre-test was administered according to assessment protocols for five selected visual skills performed in both a nonfatigued and fatigued condition. The treatment group participated in an eight-week visual training intervention programme. The purpose of this visual training programme was to train the five selected visual skills (peripheral awareness, eye-hand coordination, eyebody coordination, visual reaction time and visual-motor response time and to practice these skills during fatigued cardiovascular conditions. The post test was administered immediately after the intervention period. Interaction effects were found for three variables: peripheral awareness, eye-hand coordination and visual reaction time, so conclusions could be drawn only for eye-body coordination and visual-motor response time. No significant differences were found for visual-motor response time in the non-fatigued condition. It can be concluded that the sports vision training programme, as implemented in this study, resulted in a significant improvement in visual-motor response time of the treatment group as compared to the control group, when performing under fatigue conditions.

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20

Howard, Heidi C. "Identification of the gene responsible for peripheral neuropathy associated with agenesis of the corpus callosum". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84259.

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Peripheral neuropathy associated with agenesis of the corpus callosum (ACCPN or HMSN/ACC) is a severe polyneuropathy affecting both the peripheral nervous system and the central nervous system. It is transmitted as an autosomal recessive trait and is particularly frequent in the French Canadian population of Quebec (Canada). The disease was linked to chromosome 15 in 1996 by Dr. Rouleau's team.
We genotyped polymorphic markers in the ACCPN candidate region on chromosome 15 in over 67 patients and 200 control individuals. Observation of affected haplotypes confirmed the presence of a founder effect in the French Canadian population. Recombination analysis reduced the candidate interval to approximately 2 cM between markers D15S1040 and ACTC on chromosome 15. Linkage disequilibrium analysis suggested the gene resides nearest marker D15S1232. A physical map of the newly refined candidate region was constructed using YAC, BAC and PAC clones. These clones were used to confirm the position of candidate ESTs and genes as being either within or outside the ACCPN candidate region.
The connexin 36 gene, which was confirmed to reside within the region, was excluded as the gene responsible for ACCPN using SSCP analysis. The SLC12A6 gene was also confirmed to reside within the candidate interval and was tested for mutations using SSCP, dHPLC and sequence analyses. We found a total of four disease-specific mutations in SLC12A6, all of which are expected to truncate the KCC3 protein (the protein produced by the SLC12A6 gene). Two of the four mutations were identified in the French Canadian population; 80 French Canadian ACCPN patients are homozygous for the c.2436delG in exon 18 and one French Canadian patient is a compound heterozygote, having the c.2436delG mutation as well as the 1584_1585delCTinsG mutation in exon 11. Two additional mutations were identified in one Turkish and one Italian family in exons 22 and 15 respectively. The effects of the c.2436delG mutation on KCC3 function was studied in X. laevis oocytes and the truncated protein is not functional. Finally, collaborators at Vanderbilt University disrupted the slc12a6 gene in the mouse and found a phenotype similar to the human disease.
Identification of SLC12A6 as the gene mutated in ACCPN will allow for accurate molecular diagnosis as well as carrier testing in the French Canadian population. It is also the first step in understanding the molecular mechanism leading to the disease.

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Peterson, Erik J. "INFRARED NEURAL STIMULATION AND FUNCTIONALRECRUITMENT OF THE PERIPHERAL NERVE". Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1363640552.

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Oulad, Ben Taib Nordeyn. "Effects of hemicerebellectomy on the excitability of the motor cortex". Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209895.

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Il est bien établi que le cervelet joue un rôle déterminant sur le plan de la coordination motrice et de la préparation du mouvement. Ces rôles nécessitent impérativement une collaboration étroite entre le cervelet et le cortex moteur. La nature de ces interactions demeure mal comprise. Au cours des travaux expérimentaux présentés ici, nous nous sommes intéressés aux interactions entre le cervelet et le cortex moteur chez le rat Wistar en vue de mieux cerner les relations entre le cervelet et le cortex moteur. La mise en lumière de ces mécanismes pourrait avoir un impact sur la compréhension des fonctions du cervelet et la prise en charge des patients présentant une atteinte cérébelleuse. Dans un premier travail, nous avons étudié les interactions entre le noyau interposé du cervelet et l’excitabilité de la moelle épinière. Les effets de l’administration de tétrodotoxine (TTX, bloqueur des canaux sodiques) sur le recrutement du réflexe H ont été investigués. L’administration intranucléaire de TTX a altéré la courbe de recrutement du réflexe H sans en affecter le seuil ou l’amplitude maximale (rapport H max/M max inchangé avant et après l’administration de TTX). L’amplitude des ondes F était déprimée, avec une persistance de ces ondes diminuée et des rapports F moyen/M moyen réduits. Nous avons observé que la stimulation répétitive concomitante du nerf sciatique corrige la dépression de la courbe de recrutement du réflexe H, sans agir sur la dépression de l’onde F. Ces premiers résultats (1) ont montré que les canaux sodium sensibles à la TTX au niveau des noyaux interposés du cervelet modulent le recrutement du réflexe H, et (2) ont révélé l’existence d’une interaction entre les canaux sodium sensibles à la TTX au niveau des noyaux interposés du cervelet et l’activité afférente répétitive, ce qui n’était pas décrit jusqu’à présent. Nous avons ensuite analysé le rôle du cervelet sur la modulation des efférences corticomotrices lors d’une stimulation électrique répétitive du nerf sciatique chez le rat. Des travaux antérieurs ont en effet montré qu’une stimulation somatosensitive soutenue induit une augmentation de l'intensité de la réponse du cortex moteur de rongeurs par un mécanisme de plasticité à court terme. Jusqu'à présent, il a été considéré que l'augmentation de l’intensité des efférences motrices après la stimulation de nerf périphérique correspond à une plasticité dépendante uniquement du cortex sensorimoteur. Un total de 6 groupes de rats a été investigué. Nous avons analysé la réponse évoquée par la stimulation électrique du cortex moteur droit avant (condition basale) et après la stimulation électrique périphérique du nerf sciatique gauche chez des rats contrôles ne présentant aucune lésion cérébelleuse (pas d’intervention cérébelleuse) et chez des rats recevant une infusion d’une solution de Ringer via une sonde de microdialyse implantée dans les noyaux cérébelleux gauches. De plus, nous avons examiné les effets de (1) l'administration d'éthanol (20 mmol/L) dans les noyaux cérébelleux gauches; (2) l'administration de TTX dans les noyaux cérébelleux

gauches; (3) la stimulation électrique par stimulation cérébelleuse profonde (stimulation des noyaux interposés) sur le côté gauche; et (4) la stimulation électrique des noyaux cérébelleux du côté controlatéral. Pour la stimulation périphérique, tous les animaux ont reçu 1 heure de stimulation électrique. Les trains de stimulation ont consisté en cinq stimuli (durée de 1 stimulus: 1 ms) à une fréquence de 10 Hz. Pendant la stimulation du cortex moteur, les amplitudes pic-à-pic des réponses du muscle gastrocnémien gauche ont été analysées. Le seuil moteur (motor threshold :MT) a été défini comme l'intensité la plus basse induisant au moins 5 réponses avec une amplitude >20 µV sur 10 réponses évoquées. L'intensité utilisée était à 130 % du seuil moteur (130 % de MT). Dans la condition basale (avant la stimulation répétitive), les amplitudes des réponses motrices sont similaires dans les six groupes de rats. Chez les rats sans intervention cérébelleuse, la stimulation électrique périphérique a été associée à une augmentation significative de l’amplitude des réponses corticomotrices par rapport à la condition basale. Chez les rats avec infusion de Ringer, les réponses motrices ont augmenté de manière similaire par rapport à la condition basale. L'administration d'éthanol dans le cervelet a empêché la majoration de la réponse ipsilatérale. La même observation a été faite après l'infusion de TTX et après la stimulation électrique des noyaux cérébelleux du côté gauche. Cependant, la stimulation électrique des noyaux cérébelleux du côté droit n'a pas détérioré la modulation des efférences corticomotrices associée à la stimulation répétitive du nerf sciatique. Nous avons ensuite analysé les effets de l’hémicérébellectomie sur la modulation des activités des efférences du cortex moteur associée à la stimulation électrique répétitive du nerf sciatique chez le rat. L’hémicérébellectomie constitue un modèle de lésion aigüe étendue du cervelet. L’hémicérébellectomie a bloqué la majoration de la réponse corticomotrice, confirmant que le cervelet est un acteur-clé de cette forme de plasticité à court terme. Nous avons examiné les réflexes cutanéomusculaires au niveau du muscle plantaire des rats (1) en réponse à la stimulation cutanée isolée, et (2) en réponse à une association de stimuli cutanés avec des trains de stimuli de haute fréquence appliqués sur le cortex moteur controlatéral, avant et après la stimulation répétitive périphérique. Après une période de stimulation répétitive périphérique, l’amplitude des réponses cutanéomusculaires augmente lorsque des trains de stimulation de haute fréquence sont appliqués au niveau du cortex moteur controlatéral. Les réponses cutanéomusculaires ont aussi été examinées avec le même paradigme après hémicérébellectomie. Nous avons observé que la majoration de l’amplitude des réponses cutanéomusculaires associée aux trains de stimulation de haute fréquence après la période de stimulation répétitive périphérique a été bloquée par l’hémicérébellectomie. Nos résultats suggèrent donc que les voies passant par le cervelet sont impliquées dans le calibrage des réponses cutanéomusculaires et qu’une lésion cérébelleuse aigüe étendue altère cette fonction cérébelleuse.

Dans un travail suivant, nous avons analysé les effets de la stimulation répétitive à basse fréquence du cortex moteur (LFRSM1) (1) sur l'inhibition interhémisphérique (IHI), et (2) sur la modulation des réponses cutanéomusculaires chez des rats présentant une ablation de l’hémicervelet gauche. L’IHI a été évaluée par la méthode des stimulations pairées (technique de conditionnement), en utilisant un stimulus de conditionnement (CS) à M1 suivi par un stimulus test (TS) controlatéral. Nous avons mis en évidence que les LFRSM1 ont réduit l’IHI. La combinaison de LFRSM1 avec une stimulation répétitive périphérique a augmenté significativement l’amplitude des réponses cutanéomusculaires évoquées ipsilatéralement à l’ablation de l'hémicervelet. L'augmentation de l'intensité de la réponse cutanéomusculaire était corrélée à la réduction de l’IHI. Cependant, l’excitabilité du pool des motoneurones de la corne antérieure, évaluée par l’onde F, est restée inchangée. La conjonction des LFRSM1 avec la stimulation répétitive périphérique peut donc être utilisée pour rétablir la capacité du cortex moteur de moduler l'intensité des réponses cutanéomusculaires en cas de vaste lésion cérébelleuse unilatérale. Cette étude souligne pour la première fois le rôle potentiel des voies transcalleuses dans les déficits de la modulation corticomotrice des réponses cutanéomusculaires controlatérales à la lésion cérébelleuse aiguë étendue. Nous avons ensuite étudié les effets des stimulations électriques prémotrices de basse et de haute fréquence sur les réponses corticomotrices conditionnées, sur la facilitation intra-corticale (ICF) et sur l’excitabilité spinale chez des rats hémicérébellectomisés du côté gauche. Des trains de stimulations ont été appliqués dans la région préfrontale rFR2 (équivalente des aires prémotrices et motrices supplémentaires chez les primates) à une fréquence de 1 Hz (stimulation de basse fréquence: LFS) ou de 20 Hz (stimulation de haute fréquence: HFS). Des stimuli tests sur le cortex moteur ont été précédés par des stimuli conditionnant sur le nerf sciatique controlatéral (2 intervalles inter-stimuli – ISI- ont été étudiés: 5 ms et 45 ms): (A) à un ISI de 5 ms, le conditionnement augmente les amplitudes des potentiels évoqués moteurs au niveau du cortex moteur gauche. Cette facilitation afférente est majorée si elle est précédée par des trains de stimulation appliqués sur l’aire rFR2 ipsilatérale, et la stimulation HFS a un effet plus important que la stimulation LFS. La facilitation est plus faible au niveau du cortex moteur droit, aussi bien pour la stimulation LFS que pour la stimulation HFS, (B) à un ISI de 45 ms, les potentiels moteurs conditionnés sont déprimés en comparaison aux réponses non conditionnées (mécanisme d’inhibition afférente). Après une stimulation LFS, le degré d’inhibition est inchangé. Au niveau basal, l’inhibition est majorée au niveau du cortex moteur droit. De manière intéressante, l’inhibition afférente diminue significativement à la suite de la stimulation HFS, (C) l’ICF est déprimée au niveau du cortex moteur droit, mais est sensible à la stimulation LFS et HFS. Ces résultats (1) confirment la majoration de l’inhibition au niveau du cortex moteur controlatéral à l’ablation de

l’hémicervelet, (2) démontrent pour la première fois que le cervelet est nécessaire pour la modulation fine des amplitudes des réponses corticomotrices consécutives à la stimulation nerveuse périphérique, (3) montrent que l’application de stimulation LFS ou HFS ne modifie pas les anomalies de l’excitabilité du cortex moteur pour des ISI courts, et (4) suggèrent que pour des ISI longs, la stimulation HFS pourrait avoir des propriétés intéressantes pour la modulation de l’inhibition afférente en cas de lésion cérébelleuse étendue. Etant donné que le cervelet apparaît comme un modulateur-clé de l'activité du cortex moteur, permettant la maintenance et la modulation fine des décharges du cortex moteur, et qu’un des défauts élémentaires associés aux lésions cérébelleuses aiguës est une excitabilité réduite du cortex moteur controlatéral, nous avons évalué les effets des trains de stimulation anodale transcraniale directe (tDCS), qui produisent des changements (polarité-dépendant) des potentiels de membrane, chez des rats hémicérébellectomisés. Les trains de tDCS ont contrecarré les altérations de l’excitabilité corticomotrice controlatérale à l'ablation de l’hémicervelet. Toutefois, tant la dépression du réflexe H, que la dépression de l’onde F, sont restées inchangées avec la tDCS. Les réflexes cutanéomusculaires sont aussi restés inchangés. Les trains de tDCS ont antagonisé l’hypoexcitabilité corticomotrice induite par la stimulation à haute fréquence du noyau interposé. Nos résultats montrent que les trains de tDCS ont la capacité de moduler l’excitabilité du cortex moteur après dysfonction aigüe du cervelet. En particulier, en plaçant le cortex moteur à un niveau approprié d’excitabilité, les trains de tDCS pourraient permettre au cortex moteur de devenir plus réactif aux procédures d’apprentissage ou d’entraînement. Ceci a un potentiel clinique direct pour nos patients présentant une lésion cérébelleuse aigüe étendue. Nos travaux soulignent l’importance jouée par le cervelet dans la modulation des réponses corticomotrices chez le rat Wistar, tant pour le maintien d’un niveau approprié d’excitabilité que pour une réponse adéquate à des stimuli périphériques ou centraux. Nos résultats montrent pour la première fois que la tDCS pourrait constituer une technique de thérapie pour des patients cérébelleux présentant une dépression de l’excitabilité du cortex moteur. L’hypothèse que la tDCS pourrait contrecarrer l’hypoexcitabilité corticale chez le patient ataxique mérite d’être testée. Cette technique est peu invasive et commence à être utilisée chez l’homme.

Doctorat en Sciences médicales
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FALZONE, YURI MATTEO. "Peripheral Nervous System Involvement in Amyotrophic Lateral Sclerosis: from diagnosis to disease understanding and development of novel biomarkers". Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/128353.

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The mainstay of Amyotrophic lateral sclerosis (ALS) diagnosis is the clinical evaluation, and it can be challenging when its first manifestations overlap with those of ALS mimic disorders (ALSmd). The lack of specific diagnostic test prevents an early diagnosis. The definition of prognosis in ALS is hampered by the heterogeneity of its clinical features, with variability in survival being the most salient feature. Therefore, wet biomarkers are needed to aid clinical decision, track disease progression, and better define disease trajectories. Recent advances highlighted neurofilaments as the most promising biomarkers for ALS. In the first part of our results, we assessed serum phosphorylated neurofilament heavy chain (pNfH) in a large ALS cohort (n=219). pNfH was an independent predictor of survival for ALS and its concentration was heterogenous across the ALS phenotypes, patients with fast disease progression and a predominant upper motor neuron burden showed the highest serum concentration. Subsequently, we performed gene expression and pathways analyses, on 8 motor nerve biopsies of patients with ALS and compared with 7 motor neuropathies as controls, identifying Ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) as a potential candidate biomarker for ALS. Therefore, we tested UCHL1 in an independent large ALS and control cohorts to assess its diagnostic and prognostic performances. At the same time, we also tested serum Neurofilament light chain (NfL) and Glial fibrillary acidic protein (GFAP). In our analysis, UCHL1 resulted not promising as diagnostic biomarkers, conversely, it was an independent prognostic factor, proving itself helpful in the stratification of survival for patients with lower NfL levels. NfL consistently reached the best diagnostic performance for ALS showing almost optimal performance in discriminating ALS from healthy controls and other neurodegenerative diseases. Conversely, the diagnostic yield in distinguishing ALS from ALSmd was lower with specificity decreasing to 78.0%. As similarly observed for the pNfH, NfL concentrations were heterogenous across the ALS phenotypes and higher concentrations were detected in patients with a fast disease progression and a predominant upper motor neuron burden. Serum GFAP, a known marker of astrogliosis, differs among cognitive phenotypes, namely ALS with concomitant cognitive impairment or FTD had higher levels compared with ALS with normal cognition. Therefore, GFAP might be instrumental in tracking the occurrence of cognitive decline in ALS.
La diagnosi della Sclerosi Laterale Amiotrofica (SLA) è principalmente basata sulla valutazione clinica e può essere talvolta problematica soprattutto quando le manifestazioni cliniche sono sovrapponibili a quelle di malattie neurologiche che possono mimare la SLA. L’assenza di test diagnostici specifici limitano la possibilità di formulare la diagnosi in fase precoce di malattia. La definizione della prognosi dei malati di SLA è limitata dall’eterogeneità fenotipica della malattia e dalla sua intrinseca variabilità inter-individuale. Alla luce di tali considerazioni, eventuali biomarcatori potrebbero essere utili nel guidare decisioni diagnostiche, terapeutiche e di valutazione prognostica. Recenti evidenze di letteratura hanno individuato i neurofilamenti a catena leggera e pesante (NfL e pNfH) come i due più promettenti biomarcatori per la SLA. Nella prima parte del nostro studio, abbiamo valutato la concentrazione sierica dei pNfH in una numerosa cohorte di pazienti affetti da SLA (n=219). I nostri risultati evidenziano che in analisi multivariata i pNfH sono risultati fattori indipendenti nel predizione della sopravvivenza dei pazienti. Inoltre, la concentrazione dei pNfH è risultata eterogenea nella popolazione SLA; i valori più elevati sono stati riscontrati nei pazienti con prevalente interessamento del I neurone di moto e concomitante elevata velocità di progressione di malattia. In seguito, abbiamo effettuato un’analisi di espressione genica e sequenziale analisi di pathways su 8 nervi motori ottenuti da pazienti SLA e 7 da pazienti con neuropatia motoria considerati come controlli. Da tale analisi abbiamo indentificato UCHL1 come una proteina potenzialmente promettente come biomarcatore per la SLA. Abbiamo analizzato i valori plasmatici di tale proteina esplorandone le potenzialità diagnostiche e prognostiche, in parallelo abbiamo misurato anche i valori plasmatici di NfL, GFAP e tTAU in coorte di pazienti SLA (n=143) e di controllo. Nel nostro studio UCHL1 non si è confermato un promettente biomarcatore per la diagnosti di SLA, tuttavia è risultato essere un fattore determinante per la definizione prognostica dei pazienti stratificando ulteriormente la prognosi dei pazienti SLA con bassi valori plasmatici di NfL. Dalle nostre analisi si conferma che NfL come i migliori biomarcatori diagnostici sia per discriminare i pazienti SLA dai controlli sani (HC) e da pazienti affetti da altre malattie neurodegenerative (DEG). Tuttavia, la performance diagnostica degli NfL nel distinguere le SLA dalle patologie SLA mimic è sensibilmente ridotta con una sensibilità del 78%. Come osservato per i pNfH, anche i livelli di NfL sono più elevati in pazienti con prevalente interessamento del I neurone di moto e concomitante elevata velocità di progressione di malattia. I livelli plasmatici di GFAP riflettono i diversi gradi di interessamento cognitivo nei pazienti affetti da SLA, infatti pazienti SLA con concomitante demenza fronto-temporale o interessamento cognitivo presentavano più elevati valori di GFAP rispetto a pazienti SLA con selettivo interessamento motorio. Alla luce di questi dati GFAP potrebbe essere un biomarcatore utile per tracciare il declino cognitivo dei pazienti con SLA.

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Lindholm, Tomas. "On traumatic lesions to the spinal cord and dorsal spinal roots : factors influencing axonal regrowth across the border between the central and peripheral nervous system in rat and man /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-163-2.

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Smělý, Jiří. "Sací kanály Wankelova motoru". Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2017. http://www.nusl.cz/ntk/nusl-318690.

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This master’s thesis deals with design of intake port for turbocharged Mazda 13B-T engine with Wankel-type rotating piston motion aiming for possible modifications leading to increase of performance parameters. The main objective of this thesis is to propose appropriate modifications in order to achieve increased torque in widest possible engine speed range.

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Welin, Dag. "Neuroprotection and axonal regeneration after peripheral nerve injury". Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32819.

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Allodi, Ilary. "Changing the Intrinsic Growth Capacity of motor and sensory neurons to promote axonal growth after injury". Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96355.

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Les lesions dels nervis perifèrics provoquen paràlisis, anestèsia i pèrdua del control autonòmic de la zona afectada. Després de lesió, la part distal dels axons queda desconectat del soma i degenera, provocant la denervació dels òrgans diana. La degeneració walleriana crea un microambient favorable per al creixement axonal, alhora que la neurona canvia a un fenotip proregeneratiu. Malauradament, la manca d’especificitat de la regeneració, en termes de creixement motor i sensorial i reinnervació, és un dels grans limitats de la recuperació. Els mecanismes moleculars mplicats en la regeneració axonal i després de lesió són complexes i les interaccions entre els axons i la glia, els factors tròfics, la matriu extracel.lular i els seus receptors són fonamentals. Per aquestes raons, hem caracteritzat un model qeu ens permet comparar sota les mateixes condicions, creixement neurític motor i sensorial. Hem posat a punt un model in vitro, basat en cultius organotípics de medul.la espinal i explants de ganglis de les arrels dorsals de rates postnatals de 7 dies, embeguts en una matriu de col.lagen. Afegitn difernets factors tròfics a la matriu, hem avaluat la fiabilitat de les preparacions de gangli i de medul.la espinal. A més a més, també hem posat a punt un co-cultiu amb cèl.lules de Schwann dissociades que mimetizen millor l’ambient permissiu del nervi perifèric. Amb aquest model, hem analitzat els efectes de diferents factors tròfics que potencialment podien afavorir la especificitat de la regeneració, i com aquests factors podien ser sobre-regulats de manera diferencial per branques de nervis motors i sensorials després de la lesió. Hem observat que l’FGF-2 (18 kDa) és el factor tròfic que exerceix un efecte més selectiu en el creixement de les motoneurones espinals, tant a nivell d’elongació com d’arborització de neurites. El mecanisme que provocaia aquest efecte sembla estar relacionat amb la capacitat de l’FGF-2 d’incrementar la interacció entre l’FGFR-1 i el PSA-NCAM. Les interaccions dels dos receptors són importants durant els estadis més primerencs de la neuritogènesis, mentres que la subunitat alfa7B de les integrines estaria més relacionada amb l’estabilització de les neurites. Amb l’objectiu d’explorar amb més detall la potencial habilitat de l’FGF-2 de promoure de manera selectiva la regeneració in vivo, hem produit un vector lentiviral (LV) que sobreexpressa FGF-2 i l’hem caracteritzat in vitro i in vivo. L’addició de cèl.lules de Schwann infectades amb el LV-FGF2 en la matriu de col.lagen que cobreix els explants de gangli o les medul.les espinals, incrementa el creixement de les neurites motores però no de les sensorials en comparació als co-cultius amb LV-GFP. Per tant, la sobreexpressió de l’FGF2 mitjançant el LV és tan eficaç com l’addició directe del factor en la matriu en la promoció selective de la regeneració motora. Quan el LV-FGF2 es va injectar directament al nervi ciàtic in vivo, vam corroborar que l’FGF2 se secretava a nivell de la lamina basal de les cèl.lules de Schwann. Els nivells de FGF-2 en els homogentats de nervi ciàtic una setmana després d’injectar 1μl LVFGF- 2 eren més alts que els dels nervis injectats amb vehicle o LV-GFP. Per tant, el vector LV pot ser utilitzat in vivo per tal de verificar les troballes in vitro i per investigar amb més detall la capacitate de l’FGF2 de promoure regeneració motora. En aquest treball també hem comparat la capacitat de la glia embolcalladora olfactiva i les cèl.lules de Schwann, en donar suport a la regeneració in vitro de neurites motores i sensorials. En els co-cultius de cèl.lules de Schwann i els explants de gangli i medul.les espinals, s’observava un increment de la regeneració motora, menters que la glia embolcalladora incrementava signifiativament el creixement neurític de les neurones sensorials. Per contra, quan la glia embolcalladora s’afegia al cultiu motor, s’observava una agregació d’aquestes cèl.lules. El comportament de la glia embolcalladora podria estar determinat pel manteniment de la citoarquitectura de les medul.les espinals, on trobem astròcits i cèl.lules Schwann endògenes. Les interaccions entre la cèl.lula de Schwnn, la glia olafctòria i els astròcits, a través del complexe FGFR1-FGF2-HSPG, poden provocar agregació cel.lular. De fet, els nivells elevats d’HSPG van detectar-se al costat de la barrera, i això pot explicar el paper complex d’aquestes neurones. Els nivells elevats d HSPG és van detecar a la zona de lesió , i això pot explicar el paper quimio-repelent dels agregats cel.lulars.
Peripheral nerves injuries result in paralysis, anesthesia and lack of autonomic control of the affected body areas. After injury, axons distal to the lesion are disconnected from the neuronal body and degenerate, leading to denervation of the peripheral organs. Wallerian degeneration creates a microenvironment distal to the injury site that supports axonal regrowth, while the neuron body changes in phenotype to promote axonal regeneration. However, the lack of specificity of nerve regeneration, in terms of motor and sensory axons regrowth, pathfinding and target reinnervation, is one the main shortcomings for recovery. The molecular mechanisms implicated in axonal regeneration and pathfinding after injury are complex, and take into account the cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules and their receptors. For these reasons, we characterized a model that allows us to compare under the same conditions motor and sensory neuron regeneration. We set up an in vitro model, based on organotypic cultures of spinal cord slices and dorsal root ganglia explants from P7 rats, embedded in a collagen matrix. By adding different neurotrophic factors in the collagen matrix, we evaluated the reliability of DRG and spinal cord preparations. Moreover, we also set up a co-culture with dissociated Schwann cells to further mimic the permissive environment of the peripheral nerve. Later, we screened in vitro the different capabilities of trophic factors with promising effect on specific reinnervation of target organs after peripheral nerve regeneration. Trophic factors which promoted in vitro neuritogenesis of sensory and motor neurons were up-regulated in Schwann cells obtained from axotomized sensory and motor branches respectively. We found that FGF-2 (18 kDa) was the trophic factor that exerted the most selective effect in promoting neurite outgrowth of spinal motoneurons both in terms of elongation and arborization. The mechanism underling this effect in neuritogenesis seems related to FGF-2 enhancing the interaction between FGFR-1 and PSA-NCAM. The interaction of these two receptors is important during early stages of neuritogenesis and pathfinding, while integrin alpha7B subunit seems to play a role during neurite stabilization. With the aim to further explore the potential capacity of FGF-2 to selectiveley promote motor regeneration in vivo, we produced a lentiviral (LV) vector to overexpress FGF-2 and we characterized it in vitro and in vivo. Addition of cultured Schwann cells infected with FGF-2 into a collagen matrix embedding spinal cords or DRG significantly increased motor neurite growth but not sensory outgrowth when compared to co-cultures with LV-GFP, thus demonstrating that the LV construct was as effective as direct addition of the trophic factor to selectively promote motor neuron growth. By injecting the LV construct direclty into the sciatic nerve in vivo, we corroborated the localization of the secreted FGF-2 in the basal lamina of Schwann cells. Levels of FGF-2 from homogenated sciatic nerves one week after injection of 1μl LV-FGF-2 were higher than from nerves injected with vehicle or LV-GFP. Therefore, the LV vector can be used in vivo to verify our in vitro results and further study the capacity of FGF-2 to enhance motor nerve regeneration. In the last part of our work, we compare the abilities of Olfactory Enshealting cells and Schwann cells in sustaining in vitro motor and sensory neuritogenesis. Co-culture of cells with DRG explants and spinal cord organotypic slices was set up. SCs were promoting motoneuron growth, whereas OEC were significantly increasing neurite outgrowth in DRGs. In contrast, when OEC were added into motoneuron culture, we saw cell clusters and motoneuron outgrowth inhibition. This behaviour of OEC could be due to the maintained cytoarchitecture of the spinal cord in vitro where astrocytes and endogenous Schwann cells were also present. Interactions of SC, OEC and astrocytes through FGFR1-FGF2-HSPG complex can cause cell clustering. In fact, high levels of HSPG were found into the boundary formations, and this can explain the chemorepellent role of the cluster on neurite outgrowth.

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Lloyd, Alex. "Neuromuscular fatigue, muscle temperature and hypoxia : an integrative approach". Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/21766.

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Real world exposures to physiologically and/or psychologically stressful environments are often multifactorial. For example, high-altitude typically combines exposure to hypobaric hypoxia, solar radiation and cold ambient temperatures, while sea level thermal stress is often combined with supplementary or transient stressors such as rain, solar radiation and wind. In such complex environments, the effect of one stressor on performance may be subject to change, simply due to the presence of another independent stressor. Such differential influences can occur in three basic forms; additive, antagonistic and synergistic, each term defining a fundamental concept of inter-parameter interactions. As well as the natural occurrence of stressors in combination, understanding interactions is fundamental to experimentally modelling how multiple physiological strains integrate in their influence on or regulation of - exercise intensity. In this thesis the current literature on neuromuscular fatigue and the influence of thermal and hypoxic stress is reviewed (Chapter 1). This is followed by an outline of the methodological developments used in the subsequent experiments (Chapter 2). In the first experimental study (Chapter 3) a novel approach was adopted to investigate the combined effect of muscle cooling and hypoxia on neuromuscular fatigue in humans. The results showed that the neuromuscular system s maximal force generating capacity declined by 8.1 and 13.9% during independent cold and hypoxic stress compared to control. Force generation decreased by 21.4% during combined hypoxic-cold compared to control, closely matching the additive value of hypoxia and cold individually (22%). This was also reflected in the measurement of mechanical fatigue (electromechanical ratio), demonstrating an additive response during combined hypoxic-cold. From this study, it was concluded that when moderate hypoxia and cold environmental temperatures are combined during low intensity exercise, the level of fatigue increases additively with no interaction between these stressors. Before conducting a more complex investigation on combined stressors, a better understanding of the role of muscle temperature on central fatigue - i.e. voluntary muscle activation via the afferent signalling pathways was sought. The focus of Chapter 4 was to quantify the relationship between muscle temperature and voluntary muscle activation (central fatigue) across a wide range of temperatures. The primary finding was that different muscle temperatures can induce significant changes in voluntary activation (0.5% reduction per-degree-centigrade increase in muscle temperature) when neural drive is sustained for a prolonged effort (e.g. 120-s); however this effect is not exhibited during efforts that are brief in duration (e.g. 3-s). To further explore this finding, Chapter 5 investigated the effect of metaboreceptive feedback at two different muscle temperatures, using post-exercise muscle ischemia, on voluntary activation of a remote muscle group. The results showed that at the same perceived mental effort, peripheral limb discomfort was significantly higher with increasing muscle temperature (2% increase per-degree-centigrade increase). However any influence of increased muscle temperature on leg muscle metaboreceptive feedback did not appear to inhibit voluntary muscle activation - i.e. central control - of a remote muscle group, as represented by an equal force output and voluntary activation in the thermoneutral, contralateral leg. In Chapter 6, the psycho-sensory effects of changes in muscle temperature on central fatigue during dynamic exercise were investigated. During sustained dynamic exercise, fatigue development appeared to occur at a faster rate in hot muscle (4% increase per-degree-centigrade increase) leading to a nullification of the beneficial effects of increased muscle temperature on peak power output after a period of ~60-s maximal exercise. In support of previous studies using isometric exercise (Chapter 4 and 6), participants reported significantly higher muscular pain and discomfort in hot muscle compared to cooler muscle during dynamic exercise (2 and 1% increase per-degree-centigrade increase respectively), however this did not result in a lower power output. From Chapters 4, 5 and 6 it was concluded that in addition to faster rates of metabolite accumulation due to cardiovascular strain, it is possible that a direct sensitisation of the metaboreceptive group III and IV muscle afferents occurs in warmer muscle. This likely contributes to the reduction in voluntary muscle activation during exercise in the heat, while it may attenuate central fatigue in the cold. It was also interpreted that muscle afferents may have a similar signalling role to cutaneous sensory afferents; the latter of which are recognised for their role in providing thermal feedback to the cognitive-behavioural centres of the brain and aiding exercise regulation under thermal stress. The impact of body core and active muscle temperature on voluntary muscle activation represented a similar ratio (5 to 1 respectively) to the temperature manipulated (single leg) to non-temperature manipulated mass (rest of body) in Chapters 4, 5 and 6. This indicates that voluntary muscle activation may also be regulated based on a central meta-representation of total body heat content i.e. the summed firing rates of all activated thermoreceptors in the brain, skin, muscle, viscera and spine. Building on the initial findings of Chapter 3, Chapter 7 investigated the causative factors behind the expression of different interaction types during exposure to multi-stressor environments. This was achieved by studying the interaction between thermal stress and hypoxia on the rate of peripheral and central fatigue development during a high intensity bout of knee extension exercise to exhaustion. The results showed that during combined exposure to moderate hypoxia and mild cold, the reductions in time to exhaustion were additive of the relative effects of hypoxia and cold independently. This differs from the findings in Chapter 3, in which fatigue was additive of the absolute effects of cold and hypoxia. In contrast, combining moderate hypoxia with severe heat stress resulted in a significant antagonistic interaction on both the absolute and relative reductions in time to exhaustion i.e. the combined effect being significantly less than the sum of the individual effects. Based on the results in Chapter 7, a quantitative paradigm for understanding of systematic integration of multifactorial stressors was proposed. This is, that the interaction type between stressors is influenced by the impact magnitude of the individual stressors effect on exercise capacity, whereby the greater the stressors impact, the greater the probability that one stressor will be cancelled out by the other. This is the first study to experimentally model the overarching principles characterising the presence of simultaneous physiological strains, suggesting multifactorial integration be subject to the worst strain takes precedence when the individual strains are severe.

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Ansari, Yekta. "The Effect of Thermal Stimulation on Corticospinal Excitability". Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39328.

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This thesis describes a series of experiments to investigate the effect of thermal stimulation on corticospinal excitability using transcranial magnetic stimulation (TMS). Experiment I showed that innocuous cooling or warming of a single digit, produced short-lasting and mixed patterns of modulation only during actual thermal stimulation, with the inhibition being the most common pattern observed. In line with this finding, cooling stimulation applied to a larger area (i.e. multi-digits) produced variable but more sustained modulation in motor evoked potential (MEP) amplitude in the post-cooling phase (Exp II). Notably, the responses to cooling in terms of either suppressed or enhanced corticospinal excitability tended to be fairly consistent in a given individual with repeated applications. When examining possible sources of the observed variable MEP modulation, we found that individual characteristics such as age, sex and changes in skin temperature had no major influences. We hypothesized that the variability of responses might be related to individual differences in the excitability of intra-cortical circuits involved in sensorimotor integration. To test this hypothesis, we performed Experiment III using conditioning TMS paradigms. This experiment revealed that TMS markers of sensorimotor integration (SAI and SAF levels) were good predictors of individual variations in cooling-induced modulation in corticospinal excitability. This provided evidence supporting the role of SAI and SAF as markers to predict individual’s response to focal thermal stimulation. The identification of such predictors could enhance the therapeutic applicability of this form of stimulation in neurorehabilitation. Collectively, these findings advance our understanding of the neurophysiological basis of thermal stimulation and shed light on the development of a more rational application of neurofacilitation techniques based on afferent stimulation in clinical populations, such as stroke survivors.

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Graciani, Zódja. "Caracterização motora e funcional da paraplegia espástica, atrofia óptica e neuropatia periférica (síndrome Spoan)". Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-22032010-172509/.

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Introdução: A síndrome Spoan é uma forma de paraplegia espástica complicada de herança recessiva recentemente identificada em indivíduos originários do sudoeste do estado do Rio Grande do Norte. O quadro clínico é caracterizado por atrofia óptica congênita, paraplegia crural espástica de caráter progressivo e neuropatia axonal levando a perda da função motora em membros superiores. A caracterização fenotípica dessa doença não está completa, e não foram realizados estudos quantitativos e funcionais, que poderiam mensurar a intensidade e contribuir para a definição de uma estratégia de reabilitação. Objetivos: caracterizar o desempenho motor e as habilidades funcionais de indivíduos acometidos pela Spoan. Casuística e metodologia: participaram do estudo 61 indivíduos com diagnóstico clínico de Spoan com idade entre 5 e 72 anos. Avaliou-se a força de preensão palmar por meio do dinamômetro hidráulico de Jamar e a sensibilidade a pressão profunda e protetora dos pés e mãos por meio dos monofilamentos de náilon de Semmes-Weinstein. Definiu-se o grau de dependência dos indivíduos afetados por meio do Índice de Barthel modificado. Considerou-se para a descrição do desempenho motor: 1. quantificação da espasticidade, por meio da escala modificada de Ashworth; 2. grau de disfunção, de acordo com a escala ponderada de paraplegia espástica descrita por Schule e a escala funcional de paraplegia espástica hereditária descrita por Fink; 3. grau da capacidade de deambulação, por meio do índice de deambulação 4. grau da capacidade de sentar, por meio da escala de avaliação motora. Resultados: constatou-se fraqueza de preensão manual em todos os indivíduos e os valores obtidos indicam correlação inversa moderada entre a idade e a força manual. A sensibilidade mostrava-se anormal em 100% dos indivíduos avaliados em pelo menos seis pontos dos pés e mãos. O grau de dependência foi mínimo em 3,3%, médio em 23,3%, grave em 46,6% e total em 26,6% dos pacientes. Na escala de Schule, 60% dos indivíduos obtiveram entre 40/52 e 52/52 pontos e na escala de Fink detectou-se grau 5 (máximo) de disfunção em 71% dos pacientes. O grau de espasticidade teve uma distribuição bimodal, em média, de 30,5% com grau 1 e 37,7% grau 4. A capacidade de deambulação mostrou-se reduzida, com 83% dos indivíduos restritos a cadeira de rodas e 11% acamados. A habilidade de sentar-se estava preservada em todos os pacientes, sendo que 53% o faziam apenas com apoio. Conclusão: A síndrome Spoan é uma forma grave de paraplegia espástica hereditária, responsável por incapacidade progressiva e duradoura.
INTRODUCTION: Spoan syndrome is a complex form of spastic paraplegia of recessive inheritance recently identified in individuals from Southwest of Rio Grande do Norte state. Clinical features are characterized by congenital optic atrophy, progressive spastic paraplegia, and axonal neuropathy, resulting in severe handicap. Phenotypic description of this disease is nevertheless not complete; functional and quantitative studies, that would help planning a rehabilitation strategy, have not been undertaken. OBJECTIVES: To evaluate the motor performance and functional abilities of individual with Spoan syndrome. CASUISTIC AND METHODS: 61 individuals with confirmed diagnosis of Spoan, with ages ranging from 5 and 72 years were evaluated. Hand grip strength was measured with a Jamar hydraulic dynamometer and the sensitivity to deep pressure and protective hands and feet with Semmes-Weinstein nylon monofilaments. Functional abilities were verified by the Modified Barthel Index. For motor performance, the following procedures were performed: 1. Spasticity quantification, according to modified Ashworth scale; 2. Dysfunction level, according to the spastic paraplegia rating scale described by Schule and functional scale of hereditary spastic paraplegia described by Fink; 3. Gait ability, verified with deambulation index; 4.Sitting ability, using motor assessment scale. RESULTS: grip hand weakness was reduced in all patients, with a moderate inverse correlation between age and hand strength. Sensibility was abnormal in 100% of evaluated individuals in at least six points of hands and feet. Dependency level was minimum in 3.3%, moderate in 23.3%, severe in 46.6%, and total in 26.6% of individuals. According to Schule s scale , 60% of individuals scored between 40/52 and 52/52 points; in Fink s scale,71% achieved level 5 (maximum) of dysfunction. Spasticity level had a bimodal distribution, with 30,5% achieving level 1 and 37,7% level 4. Gait ability was reduced, with 83% of individuals being wheelchair bound and 11% bedridden. Sitting ability was preserved in all patients, but 53% were able to sit only with support. CONCLUSION: Spoan syndrome is a severe form of hereditary spastic paraplegia that is responsible for progressive and long lasting handicap.

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Narayan, Sreenath. "REANIMATION OF A DENERVATED MUSCLE USING UPPER MOTONEURON INJURED LOWER MOTONEURONS IN SPINAL CORD INJURY PATIENTS: A RAT MODEL". online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1133754830.

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Pereira, Gleber. "Co-ordination and fatigue of countermovement jump /". Rio Claro : [s.n.], 2007. http://hdl.handle.net/11449/100397.

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Resumo: O objetivo principal desta tese foi investigar a causa e a conseqüência da fadiga em countermovement jumps realizados em diferentes razões de esforço e pausa. Esses objetivos foram testados utilizando dois estudos experimentais. O primeiro estudo comparou as causas da fadiga em protocolos de fadiga de curta (=10 min) e longa duração (=20 min), manipulando as durações da pausa entre countermovement jumps. Os resultados indicaram que, após a realização do protocolo de fadiga de curta duração, houve redução da contração isométrica voluntária máxima para extensão do joelho acompanhada por fadiga central e periférica. Por outro lado, após a realização do protocolo de fadiga de longa duração, a redução da contração isométrica voluntária máxima para extensão do joelho foi associada apenas à fadiga periférica. No segundo estudo foi utilizado um protocolo de fadiga para o sistema neuromuscular similar ao primeiro estudo, tendo como objetivo investigar o padrão de movimento sob fadiga. O tempo e a seqüência da relação inter-segmental do movimento e da ativação muscular permaneceram inalteradas sob a condição de fadiga. Entretanto, alguns ajustes no controle de countermovement jumps realizados sob a condição de fadiga foram observados, provavelmente na tentativa de manter a altura do salto vertical. Entre alguns ajustes, é possível destacar um aumento na flexão das articulações e na duração do salto vertical. Esses resultados foram similares independentemente da razão de esforço e pausa utilizada para induzir fadiga em countermovement jumps. Considerando ambos os estudos experimentais, os resultados da presente tese sugerem que a causa da fadiga em countermovement jumps é tarefa-dependente. Isso significa que dependendo do protocolo de indução de fadiga utilizado, a causa da fadiga pode ser alterada de central para periférica, por exemplo... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: This thesis explored the cause of fatigue in countermovement jump performed under different intensities and its influence upon movement pattern. These aims were tested using two experimental studies. The first one aimed to compare the causes of fatigue development during a short- (=10 min) and a long-term (=20 min) countermovement jump protocols through the manipulation of resting interval. The results indicated that after short-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by central and peripheral fatigue. On the other hand, after long-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by peripheral fatigue. The second study used similar exercise protocol to induce fatigue on neuromuscular system. It was aimed to investigate the movement pattern of countermovement jump throughout fatigue exercise protocols. The timing and sequencing of inter-segmental movement and of muscle activation remained relatively unaltered under fatigue. However, in order to sustain required jump height, few adjustments were performed on control and on coordination of fatigued jumps, such as increased joint flexion and earlier initiation of joint extension. This result was quite similar irrespective of fatigue-induced exercise intensities. Considering both experimental studies, the results of present thesis suggest that the cause of fatigue in countermovement jump is task-dependent in which depends on what fatigue protocol is used, thereby the cause of fatigue can move from one site to another. Even with the neuromuscular system impaired, there was not change on the movement pattern of countermovement jump, irrespective of exercise duration and cause of fatigue. However, adjustments on control and coordination of countermovement jump were performed in order to compensate the force loss and to maintain the targeted jump height.
Orientador: Eduardo Kokubun
Coorientador: José Angelo Barela
Banca: André Luiz Félix Rodacki
Banca: Ana Maria Forti Barela
Banca: Carlos Ugrinowistch
Doutor

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Pereira, Gleber [UNESP]. "Co-ordination and fatigue of countermovement jump". Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/100397.

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Made available in DSpace on 2014-06-11T19:30:52Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-07-26Bitstream added on 2014-06-13T19:19:34Z : No. of bitstreams: 1 pereira_g_dr_rcla.pdf: 601547 bytes, checksum: 78fe39c887efbb78c46303cff6e30a46 (MD5)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
O objetivo principal desta tese foi investigar a causa e a conseqüência da fadiga em countermovement jumps realizados em diferentes razões de esforço e pausa. Esses objetivos foram testados utilizando dois estudos experimentais. O primeiro estudo comparou as causas da fadiga em protocolos de fadiga de curta (=10 min) e longa duração (=20 min), manipulando as durações da pausa entre countermovement jumps. Os resultados indicaram que, após a realização do protocolo de fadiga de curta duração, houve redução da contração isométrica voluntária máxima para extensão do joelho acompanhada por fadiga central e periférica. Por outro lado, após a realização do protocolo de fadiga de longa duração, a redução da contração isométrica voluntária máxima para extensão do joelho foi associada apenas à fadiga periférica. No segundo estudo foi utilizado um protocolo de fadiga para o sistema neuromuscular similar ao primeiro estudo, tendo como objetivo investigar o padrão de movimento sob fadiga. O tempo e a seqüência da relação inter-segmental do movimento e da ativação muscular permaneceram inalteradas sob a condição de fadiga. Entretanto, alguns ajustes no controle de countermovement jumps realizados sob a condição de fadiga foram observados, provavelmente na tentativa de manter a altura do salto vertical. Entre alguns ajustes, é possível destacar um aumento na flexão das articulações e na duração do salto vertical. Esses resultados foram similares independentemente da razão de esforço e pausa utilizada para induzir fadiga em countermovement jumps. Considerando ambos os estudos experimentais, os resultados da presente tese sugerem que a causa da fadiga em countermovement jumps é tarefa-dependente. Isso significa que dependendo do protocolo de indução de fadiga utilizado, a causa da fadiga pode ser alterada de central para periférica, por exemplo...
This thesis explored the cause of fatigue in countermovement jump performed under different intensities and its influence upon movement pattern. These aims were tested using two experimental studies. The first one aimed to compare the causes of fatigue development during a short- (=10 min) and a long-term (=20 min) countermovement jump protocols through the manipulation of resting interval. The results indicated that after short-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by central and peripheral fatigue. On the other hand, after long-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by peripheral fatigue. The second study used similar exercise protocol to induce fatigue on neuromuscular system. It was aimed to investigate the movement pattern of countermovement jump throughout fatigue exercise protocols. The timing and sequencing of inter-segmental movement and of muscle activation remained relatively unaltered under fatigue. However, in order to sustain required jump height, few adjustments were performed on control and on coordination of fatigued jumps, such as increased joint flexion and earlier initiation of joint extension. This result was quite similar irrespective of fatigue-induced exercise intensities. Considering both experimental studies, the results of present thesis suggest that the cause of fatigue in countermovement jump is task-dependent in which depends on what fatigue protocol is used, thereby the cause of fatigue can move from one site to another. Even with the neuromuscular system impaired, there was not change on the movement pattern of countermovement jump, irrespective of exercise duration and cause of fatigue. However, adjustments on control and coordination of countermovement jump were performed in order to compensate the force loss and to maintain the targeted jump height.

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Basu, Debaleena. "Neural Mechanisms underlying the planning of sequential saccades". Thesis, 2018. https://etd.iisc.ac.in/handle/2005/4076.

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Saccades are rapid eye movements that we continually make (about 2-3 times per second) to look around and scan our visual environment. Though we effortlessly execute saccadic eye movements all the time, they are not just reflexive movements; saccades have been shown to involve multifaceted cognitive control mechanisms. This property of saccades, combined with the fact that saccadic parameters are easily measurable, and that the neural circuitry for saccade generation is fairly well established, has established saccadic eye movements to be an excellent tool to study motor planning and decision-making. However, much of the work done on saccade planning has been limited to understanding the production of single saccades. Natural behavior entails making multiple saccadic movements in a sequence to achieve day-to-day tasks such as reading a book. How are sequential saccades planned? This question forms the broad theme of this thesis. The neural correlates of sequential saccade planning were scouted for in the macaque frontal eye field (FEF), a prefrontal area containing neuronal populations that undertake saccadic decision-making. Visual-salience neurons of the FEF have been shown to encode targets for upcoming saccades and movement-related neurons of the FEF have been shown to control the time of saccade initiation, providing a good link between neural activity and behaviorally measured reaction times. However, much of the neural underpinnings of saccade programming in the FEF have been uncovered using tasks involving single, isolated saccades. Motivated by this, I explored the mechanisms by which FEF neurons contributed to the programming of saccade sequences for this thesis, using single-unit electrophysiological recordings from the FEF of two macaques as they performed a sequential saccade task. Sequential saccade programming can, in principle, operate through two major modes: serial or parallel. Behavioral measures, like short inter-saccadic intervals, strongly indicate that multiple saccade plans can proceed in parallel. However, direct neural evidence of parallel programming in the FEF neuronal population that strongly link to behavior, i.e. movement neurons, is lacking. First, I show that FEF movement-related activity can start ramping-up for the second saccade before the first saccade execution is complete, and much before visual feedback from the first saccade can reach FEF, thereby providing neural correlates of parallel programming of sequential saccades. Perceptual processing in the FEF has been shown to precede motor processing in visual search tasks, and consistent with that notion, FEF neurons with visual activity were also able to augment activity related to the second target whilst the first saccade plan was still underway. After finding neural evidence of parallel programming, I characterized the limits of parallel programming. Numerous studies have shown that when two motor plans overlap closely, processing bottlenecks arise to inhibit the programming of the second plan, and is behaviorally manifested by the progressive lengthening of the second task reaction time, as the temporal gap between the two tasks decreases. This feature of increase in the second task latency has been observed in sequential saccade tasks as well. Neural correlates of processing bottlenecks were found in the responses of FEF movement neurons, wherein for the second saccade plan, the rate of the growth of activity was perturbed and the threshold of saccade initiation was increased, in a degree proportional to the level of concurrence of the two saccade plans. The locus of processing bottlenecks was found to be at the level of FEF movement-related neurons, whereas the activity of the visual neurons indicated that visual processing for perceptually simple tasks might constitute a pre-bottleneck stage. Evidence of activity perturbations was also found for the first saccade plan, supporting capacity-sharing theories of processing bottlenecks, as opposed to single-channel bottleneck theories which postulate that only the second plan is gated by inhibitory control while the first can pass unabated. Together, the results suggest that processing bottlenecks in sequential saccades originate in the partitioning of the brain’s limited processing ‘capacity’ by simultaneously active motor plans, due to which, inhibitory control is applied on both the first and second saccade plans, to prevent straining of the aforesaid capacity. Finally, I have examined peripheral signatures of sequential saccade planning. Recent studies using single saccade paradigms have shown that the function of FEF as a center of cognitive control is not limited to saccade eye movements, but can be generalized to the control of eye-head gaze shifts. Rapid presaccadic recruitment of dorsal neck muscle activity has been shown to occur after FEF both with single-unit microstimulation and trans-cranial magnetic stimulation, even under head-restrained conditions where no overt head movement is being brought about by the neck muscles. To investigate whether such presaccadic recruitment occurs during sequential saccade planning or is gated out by inhibitory control, I recorded electromyographic (EMG) activity of motor units of the dorsal neck muscle as macaques performed the same sequential saccade task used for neural recordings. Neck muscle EMG showed leakage of FEF planning signals even for sequential saccades: peripheral correlates of parallel programming and processing bottlenecks were observed, with the activity mirroring that of FEF movement neurons. The correspondence of the results between the FEF and periphery suggest that a tight link exists between the eye and head systems, validating the hypothesis of a common gaze command originating in the FEF. The rapid recruitment of neck muscle activity observed for the second saccade before the completion of the first, also suggested that inhibitory control gates like basal ganglia do not preferentially intercept sequential saccade signals in the FEF-neck muscle circuit. In summary, the results in this thesis provide direct neurophysiological evidence of behaviorally established features of sequential saccade planning such as parallel programming and processing bottlenecks. The fact that signatures of FEF movement responses can be captured at the level of the dorsal neck muscle suggests that the functional channel connecting FEF and the motor periphery is preserved even during sequential saccade planning and allows central responses to rapidly pass downstream by default, and perhaps prepare for an anticipated head movement in conjunction with the upcoming saccade. In cases where no head movement is elicited or where the head is restrained, inhibitory control mechanisms might come into play later and prevent supra-threshold rise of neck muscle activity.

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Rungta, Satya Prakash. "Central and Peripheral Correlates of Motor Planning". Thesis, 2017. http://etd.iisc.ac.in/handle/2005/3092.

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A hallmark of human behaviour is that we can either couple or decouple our thoughts, decision and motor plans from actions. Previous studies have reported evidence of gating of information between intention and action that can happen at different levels in the central nervous system (CNS) involving the motor cortex, subcortical structures such as the basal ganglia and even in the spinal cord. In my research I examine the extent of this gating and its modulation by task context. I will present results obtained by data collected from (a) neck muscles and neural recording from frontal eye field (FEF) in macaque monkeys and (b) putative motor units (MUs) from high density electrode arrays using surface EMG signals in human to delineate the type of information that leaks into muscles in the periphery when subjects are involved in preparing eye and hand movements, respectively, and its modulation by task context Overall, my results reveal that we can assess some aspects of central planning in the activity of motor units Further, the recruitment of these motor units depend on task context.

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Rungta, Satya Prakash. "Central and Peripheral Correlates of Motor Planning". Thesis, 2017. http://hdl.handle.net/2005/3092.

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A hallmark of human behaviour is that we can either couple or decouple our thoughts, decision and motor plans from actions. Previous studies have reported evidence of gating of information between intention and action that can happen at different levels in the central nervous system (CNS) involving the motor cortex, subcortical structures such as the basal ganglia and even in the spinal cord. In my research I examine the extent of this gating and its modulation by task context. I will present results obtained by data collected from (a) neck muscles and neural recording from frontal eye field (FEF) in macaque monkeys and (b) putative motor units (MUs) from high density electrode arrays using surface EMG signals in human to delineate the type of information that leaks into muscles in the periphery when subjects are involved in preparing eye and hand movements, respectively, and its modulation by task context Overall, my results reveal that we can assess some aspects of central planning in the activity of motor units Further, the recruitment of these motor units depend on task context.

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"Ultrasound Modulation of the Central and Peripheral Nervous System". Doctoral diss., 2015. http://hdl.handle.net/2286/R.I.34846.

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abstract: Noninvasive neuromodulation could help treat many neurological disorders, but existing techniques have low resolution and weak penetration. Ultrasound (US) shows promise for stimulation of smaller areas and subcortical structures. However, the mechanism and parameter design are not understood. US can stimulate tail and hindlimb movements in rats, but not forelimb, for unknown reasons. Potentially, US could also stimulate peripheral or enteric neurons for control of blood glucose. To better understand the inconsistent effects across rat motor cortex, US modulation of electrically-evoked movements was tested. A stimulation array was implanted on the cortical surface and US (200 kHz, 30-60 W/cm2 peak) was applied while measuring changes in the evoked forelimb and hindlimb movements. Direct US stimulation of the hindlimb was also studied. To test peripheral effects, rat blood glucose levels were measured while applying US near the liver. No short-term motor modulation was visible (95% confidence interval: -3.5% to +5.1% forelimb, -3.8% to +5.5% hindlimb). There was significant long-term (minutes-order) suppression (95% confidence interval: -3.7% to -10.8% forelimb, -3.8% to -11.9% hindlimb). This suppression may be due to the considerable heating (+1.8°C between US/non-US conditions); effects of heat and US were not separable in this experiment. US directly evoked hindlimb and scrotum movements in some sessions. This required a long interval, at least 3 seconds between US bursts. Movement could be evoked with much shorter pulses than used in literature (3 ms). The EMG latency (10 ms) was compatible with activation of corticospinal neurons. The glucose modulation test showed a strong increase in a few trials, but across all trials found no significant effect. The single motor response and the long refractory period together suggest that only the beginning of the US burst had a stimulatory effect. This would explain the lack of short-term modulation, and suggests future work with shorter pulses could better explore the missing forelimb response. During the refractory period there was no change in the electrically-evoked response, which suggests the US stimulation mechanism is independent of normal brain activity. These results challenge the literature-standard protocols and provide new insights on the unknown mechanism.
Dissertation/Thesis
Doctoral Dissertation Bioengineering 2015

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38

Hsieh, Hsiu-Min, i 謝秀敏. "fMRI Studies of Central Motor Plasticity on Patients With Upper Limb Peripheral Nerve Injury". Thesis, 2001. http://ndltd.ncl.edu.tw/handle/96434762679953355733.

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碩士
國立陽明大學
神經科學研究所
89
To examine the reorganization of human cortical area in motor system, it is important to establish the normal subjects activation pattern and then apply to clinical patients by using non-invasive functional MRI(fMRI). In this study, we start 1) to elucidate the motortotopy in the human primary sensorimotor cortex responds to specific single joint movement (simple task), 2) to investigate the effect of patients with brachial plexus injury after intercostal-musculocutaneous nerve crossing in the primary sensorimotor cortex, 3) to explore the transcallosal inhibition pattern in the human motor system while execute unilateral hand movement, 4) to dissect the effect of patients with one upper extremity paralysis influence the transcallosal inhibition pattern when their execute the same movement with unaffected hand. The data of this fMRI study demonstrated that motortotopy existed in human primary sensorimotor cortex and patients with brachial plexus injury showed plasticity in this area. Besides, normal transcallosal inhibition also was established in ipsilateral primary sensorimotor area and patients with one upper extremity paralysis exhibited a relative deactivation in supplementary motor area, cingulated motor area, and caudate. This could result from loss of transcallosal inhibition which hypotheses that unilateral hand movements are associated with contralateral cerebral activation and ipsilateral cerebral deactivation and reorganization of the motor system. Our results offer the opportunity to look into the phenomenon of plasticity in adult human brain and to exploit the functional neuroimage technique for clinical study.

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Candeias, Rui Dinis Teodoro. "Evaluation of motor neuron excitability by CMAP scanning with modulated current". Master's thesis, 2014. http://hdl.handle.net/10362/14288.

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It is important to have better evaluation and understanding of the motor neuron physiology, with the goal to early and objectively diagnose and treat patients with neurodegenerative pathologies. The Compound Muscle Action Potential (CMAP) scan is a non-invasive diagnosis technique for neurodegenerative pathologies, such as ALS, and enables a quick analysis of the muscle action potentials in response to motor nerve stimulation. This work aims to study the influence of different pulse modulated waveforms in peripheral nerve excitability by CMAP scan technique on healthy subjects. A total of 13 healthy subjects were submitted to the same test. The stimuli were applied in the medium nerve on the right wrist and electromyography signal collected on the Abductor Pollicis Brevis (APB) muscle surface on the right thumb. Stimulation was performed with an increasing intensities range from 4 to 30 mA, with varying steps, 3 stimuli per step. The procedure was repeated 4 times per subject, each repetition using a different single pulse stimulation waveform: monophasic square, monophasic triangular, monophasic quadratic and biphasic square. Results were retrieved from the averaging of the stimuli on each current intensity step. The square pulse needs less current intensity to generate the same response amplitude regarding the other waves and presents a more steep curve slope and this effect is gradually decreasing for the triangular and quadratic pulse,respectively, being the difference even more evident regarding the biphasic pulse. The control of the waveform stimulation pulse allows varying the stimulusresponse curve slope.

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Tsai, Min-Ru, i 蔡旻儒. "Changes of Intracortical Inhibition and Facilitation at Primary Motor Cortex in Patients with Peripheral Neuropathy". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/2zu422.

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Tu, Hui-Chin, i 涂惠靖. "The Effects of EGCG on Motor Neurons in the Lower Brain Stem Following Peripheral Nerve Injury". Thesis, 2004. http://ndltd.ncl.edu.tw/handle/42307122688728246344.

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碩士
國立臺灣大學
解剖學研究所
92
Peripheral nerve injury would alter nitric oxide synthase activity to cause neuronal degeneration or cell death via the overproduction of nitric oxide and impingement on metabolic pathways of related neurochemicals. Recent studies have shown that (-)-epigallocatechin gallate (EGCG), one of the green tea polyphenols, has a strong antioxidant property. It could attenuate hypoxia-induced nerve injuries by decreasing the production of free radicals and lipid peroxidation. The present study, by using histochemical and immunohistochemical methods, aimed to explore whether EGCG treatment might affect the diversion or provide neuroprotection of motor neurons and neuroglia cells of the hypoglossal nucleus (HN) and of the dorsal motor nucleus (DMN) in the lower brainstem of young albino rats following crush injury (CI). Thus, experimental animals were divided into 4 groups with 12 in each. Unilateral (left-sided) hypoglossal and vagus nerve at the level of mid-digastric muscle and of bifurcation of common carotid artery, respectively, was crushed for 30 seconds. They were received an injection of 10, 25, 50 mg/kg EGCG or saline 30 min prior to CI. One to 6 days after CI, same dosages of EGCG or saline were applied to experimental animals. They were then allowed to survive for 3, 7, 14, and 28 days, respectively. The present results showed that the percentage and optical density of nNOS expression in motor neurons increased to peak at 7 days after CI in HN then tend to decrease; but progressively lean to increase in DMN. The expression of ChAT in HN reaching its nadir at 3 days after CI then progressively to increase; but incline to decrease in DMN at 7 days, then followed by the decrease with time points and reached its nadir at 28 days. The expression of CGRP in HN peaked at 3 days after CI, then progressively decreased at 7 days but tended to increase at 14 days after that return to normal condition. As regards to the neuroglial cells, the expression of OX42 and GFAP in the microglia and astrocyte peaked at 7 days and then tended to decrease with various time points. The percentage and optical density of nNOS expression in motor neurons decreased following high dosages (25, 50mg/kg) of EGCG treatment, followed by the increase of the expression of ChAT and decrease of CGRP following CI. In addition, the expression of immunoreactivity in the neuroglial cells also decreased. In conclusion, motor neurons in the HN tended to respond to the high dosages (25, 50 mg/kg) of EGCG treatment following CI; this result is comparable to the effect of acute hypoxia on the nodose ganglion of rats in our previous study. However, the dosage effect was found only in DMN following ceiling dosage (50 mg/kg) of EGCG treatment. Although we do not know the detailed mechanism for the recovery potentiality of motor neurons in these two nuclei, the discrepancy might be due to both nuclei endorse with different functional components. The current study provides the first morphological evidence that EGCG might have protective effect on motor neurons and neuroglial cells in the lower brainstem of rats following CI.

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Creff, Natalie Eliane. "Time course of trophic factor expression in the proximal and distal stumps of transected peripheral motor nerve /". 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014720453&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Hwang, Chiao-wen, i 黃巧雯. "Electrophysiological Studies on Peripheral Neuropathy in Rats:Comparison of Conventional Nerve Conduction Studies and Magnetic Motor Root Stimulation". Thesis, 2006. http://ndltd.ncl.edu.tw/handle/24541285606245943567.

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碩士
國立中山大學
生物科學系研究所
94
Numerous mechanisms contribute to peripheral nerve injuries such as chemical intoxication, compression, stretching and avulsion, which usually result in severe damage to the sensory and motor functions. The current approaches for evaluating nerve regeneration include expression analysis of molecular markers, histological analysis, behavior testing and electrophysiological studies. The aim of this study is to compare the diagnostic efficacy using the recently developed magnetic stimulation approach with that of conventional electrical stimulation method in different models of peripheral neuropathy and to compare in terms of latency and amplitude of the evoked response by electrical and magnetic stimulation. Adult male Sprague Dawley rats (250-300 g, n = 24) were divided into three groups: (1) control group, (2) sciatic nerve ligation group and (3) acrylamide intoxication group. The electrophysiological studies were carried out 3 days before ligation and every 7 days after ligation for 4 weeks. The measurements included amplitude and onset latency of maximal compound nerve action potential (CMAP) in branches of sciatic nerve (nerves to the gastrocnemius, tibialis anterior), motor nerve conduction velocity, H-reflex, F-wave, amplitude and onset latency of motor evoked potential by lumbosacral motor root magnetic stimulation, and denervation by electromyography (gastrocnemius, tibialis anterior). The results from studies using magnetic and electrical stimulation showed prominent reduction of CMAP amplitude in rats of sciatic nerve ligation and acrylamide intoxication group. The CMAP amplitude measured by magnetic stimulation was 76~85% of that by electrical stimulation. By either magnetic stimulation or electrical stimulation, there was no significant difference in the mean onset latency of CMAP between control and neuropathy groups. Volume conduction accounts for the interference of waveform and error is inevitable. Because of the short distance of hind limb of the rat, the nerve conduction velocity (NCV), H-reflex and F-wave could not be determined using magnetic stimulation. In contrast, electrophysiological analysis by electrical stimulation revealed slowed NCV, prolonged or absent H-reflex and F-wave in animals of neuropathy groups. Electromyography showed prominent denervation potentials over the sampling muscles in both models. In conclusion, magnetic stimulation of lumbosacral motor root is non-invasive and convenient. However, further improvement and establishment of basic parameters are required to facilitate a reliable tool in evaluation of peripheral nerve injury.

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張宏名. "Effects of peripheral nerve injury along with hypoxia on the motor neurons,sensory neurons and glia cells in rats". Thesis, 2001. http://ndltd.ncl.edu.tw/handle/02431824437303005545.

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博士
國立臺灣大學
解剖學暨細胞生物學研究所
89
Either peripheral nerve injury or hypoxia will alter the NMDA receptor activity and result to neuronal degeneration or cell death via the over production of nitric oxide and affecting the metabolic pathways of related neurochemicals. By using the histochemical and immunohistochemical methods, the present study was aimed to determine the relationship between the neurochemical expression and neuronal degeneration of motor neurons, sensory neurons and glia cells under peripheral nerve injury along with hypoxia treatment. This study was also thought to explore whether the extra-administration of anti-oxidant (i.e. melatonin) will exert its neuroprotective effect on the lesioned neurons. Firstly, the acute high altitude (10000 m) hypoxic exposure was selected as the experimental paradigm to determine the effect of hypoxia on the expression patterns of related neurochemicals of sensory and motor neurons. The results revealed that after acute hypoxia treatment, the nitric oxide synthase (NOS), NMDA receptor as well as the calcitonin gene-related peptide immunoreactivities in the nodose ganglion were up-regulated, while the cytochrome oxidase (an endogenous metabolic marker) and the acetylcholinesterase histochemical staining were down-regulated. Significant neuronal loss was detected in the nodose ganglion 2 weeks following acute hypoxic exposure. On the contrary, acute hypoxia did not cause any noticeable changes in lower brainstem motor neurons bearing different functional component. Based on these results, we suggest that acute hypoxia will induce NMDA receptor mediated NOS activation in the sensory neuron, by excessive generation of free radicals and disturbing the energy metabolic pathway and neurotransmitter function, directly lead to neuronal damage or cell death. Furthermore, the peripheral nerve injury coupled with hypoxia was adopted as the double injury model to determine and compare the related neurochemical expression among the lower brainstem motor neurons bearing different functional component. The results indicated that following unilateral transection of the vagal and hypoglossal nerves, the NOS immunoreactivities were drastically increased in the lesioned nuclei. The extent of NOS up-regulation was positively correlated with the severity of neuronal damage. Besides, with the over production of nitric oxide, peripheral nerve injury and hypoxia will also suppress the reactivities of cytochrome oxidase, choline acetyltransferase as well as the Mn-superoxide dismutase (an anti-oxidant enzyme). On the other hand, axotomy along with hypoxia will cause the microglia and astrocyte activation within the lesioned nuclei as revealed by the GSA-IB4 lectin binding method and the glia fibrillary acidic protein immunohistochemistry, respectively. The expression patterns of related neurochemicals, activated status of glia cells and the numbers of neuronal loss were all more significant in the double injury treated rats as compared with those of normoxic ones. Based on these results, we suggest that peripheral nerve injury along with hypoxia will contribute to the severer neuronal damage via the over activation of NOS, which could subsequently broke the metabolic pathway, neurotransmitter function as well as the balanced status of the free radical/ anti-oxidative defense system. Results of the effects of melatonin on the acute hypoxia or peripheral nerve injury were indicated that melatonin would indeed suppress the NOS expression and reduce the neuronal demage in the lesioned neurons. The suppressive effect of melatonin on the NOS expression was dose dependent. The present study not only provides the first morphological evidence concerning the neuroprotective effect of melatonin but also increases the current knowledge for the therapeutic use of melatonin as a clinical trial to forestall the related neuropathies induced by hypoxia or peripheral nerve injury. In summary, by the use of acute hypoxia or peripheral nerve injury along with hypoxia as experimental models, the present study was clearly demonstrated the relationship between the related neurochemical expression and neuronal damage in the sensory neurons, motor neurons and glia cells. The results obtained from the present study will not only help us to better understand the physiological significance of hypoxia on the peripheral nerve injury, but also document the possible functional roles of related neurochemicals during the process of neuronal degeneration.

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Tsung-Hsun, Hsieh, i 謝宗勳. "Modulation of Motor Evoked Potentials (MEPs) and H-reflexes after Peripheral Nerve Stimulation in Individuals with Sensory Impairment following SCI". Thesis, 2004. http://ndltd.ncl.edu.tw/handle/38207643581477853655.

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碩士
長庚大學
復健科學研究所
92
Somatosensory input was required for accurate motor performance and for new motor skill learning. In humans, above motor threshold peripheral nerve stimulation resulted in an increased excitability of the motor pathway to the stimulated body parts. The purpose of this study was to investigate whether peripheral sensory afferents was essential in facilitation of motor pathway by electrical stimulation. Eight subjects with sensory impairment following SCI and nine healthy subjects were recruited. Motor evoked potentials (MEP), silent period(SP) elicited by 120% motor threshold transcranial magnetic stimulation (TMS), and H-reflex elicited by median nerve stimulation were recorded on flexor carpi radialis (FCR) muscle before, during, immediately and 30 minutes after repetitive electrical stimulation (25 Hz, on/off=800ms/ 800 ms) on median nerve. In healthy subjects, the averaged amplitude of MEP increased to 154±29% of initial (P=0.01) after repetitive electrical stimulation. This increment became statically non-significant 30 min after the stimulation stopped. In subjects with SCI, the MEP did not change. The H-reflex and low frequency depression ratio did not change in both subjects. We concluded that the sensory afferent input was essential to facilitate the corticomotoneuronal excitability during peripheral nerve stimulation.

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Wang, Chao-Ting, i 王昭鼎. "A Study of Automobile Businesses Customer Relationship Management (CRM) with its Peripheral Businesses development ─A Case of Taiwan Yulon Motor Corporation". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/55980980420341774286.

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碩士
中原大學
企業管理研究所
91
The purpose of this research in understanding the competence of Taiwan automobile business environments, and the strategy planning of Taiwan car companies and their peripheral companies in Customer Relationship Management (CRM). By using the CRM strategies of mother company and information system, in order to satisfy the customers “Moving with Convenience,” also provide full range service, products difference, market segmentation, ensure the advantage of competence. In year 2000, Yulon Motor Group base on the 50% of automobile market share, starting the company Third stage (III) reengineering program. The peripheral business, being the stretch policy of Group’s Moving Value Chain (MVC) strategy, included: auto clinic, used car sales, car leasing, travel agent, insurance, financial loan, publisher, call center, high-tech products and integration information system. Above all focus on satisfies the customers, while they are driving & moving. Due to the complexity and variety of automobile industry, we need a systemize analysis and information platform, in order for manager integrate relative strategies efficiently. By common sharing resources, dual communicate with headquarter system, integrate down-stream business and peripheral value chain, create enterprise re-engineering process. Service all customers, by using electrical analytic data; improve customer’s royalty and satisfaction, finding potential business opportunities. According to customer’s requirements, develop differential products from the competitors; ensure the long-term competing advantage of company. Above mentioned automobile business characteristics, we can realize they have certain level of interactions among with social communities, enterprises and individuals. So how to enhance the competence and development of Taiwan local automobile business, the schools, enterprises and government, should concern this subject.

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Roy, Francois D. "Associative plasticity and afferent regulation of corticospinal excitability in uninjured individuals and after incomplete spinal cord injury". Phd thesis, 2009. http://hdl.handle.net/10048/632.

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Cortical representations are plastic and are allocated based on the proportional use or disuse of a pathway. A steady stream of sensory input maintains the integrity of cortical networks; while in contrast, alterations in afferent activation promote sensorimotor reorganization. After an incomplete spinal cord injury (SCI), damage to the ascending and/or descending pathways induces widespread modifications to the sensorimotor system. Strengthening these spared sensorimotor pathways may be therapeutic by promoting functional recovery after injury. Using a technique called transcranial magnetic stimulation (TMS), we show that the leg motor cortex is facilitated by peripheral sensory inputs via disinhibition and potentiation of excitatory intracortical circuits. Hence, in addition to its crucial role in sensory perception, excitation from peripheral sensory afferents can reinforce muscle activity by engaging, and possibly shaping, the activity of the human motor cortex. After SCI, the amount of excitation produced by afferent stimulation reaching the motor cortex is expectantly reduced and delayed. This reduction of sensory inflow to the motor cortex may contribute to our findings that cortical inhibition is down-regulated after SCI, and this compensation may aid in the recruitment of excitatory networks in the motor cortex as a result of the damage to its output neurons. By repeatedly pairing sensory inputs from a peripheral nerve in the leg with direct cortical activation by TMS, in an intervention called paired associative stimulation, we show that the motor system can be potentiated in both uninjured individuals and after SCI. In the uninjured subjects, we show that in order to produce associative facilitation, the time window required for coincident activation of the motor cortex by TMS and peripheral sensory inputs is not as narrow as previously thought (~100 vs. ~20 ms), likely due to the persistent activation of cortical neurons following activation by TMS. The potential to condition the nervous system with convergent afferent and cortical inputs suggests that paired associative stimulation may serve as a priming tool for motor plasticity and rehabilitation following SCI.

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Bořilová, Karolína. "Elektromyografické a klinické hodnocení vinkristinem indukované periferní neuropatie u pediatrických pacientů po dokončení léčby akutní lymfoblastické leukemie a korelace s Bruinkins-Oseretsky Test of Motor Proficiency - second edition". Master's thesis, 2020. http://www.nusl.cz/ntk/nusl-435228.

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Title: Electromyographic and clinical evaluation of vincristine-induced peripheral neuropathy in pediatric patients after treatment of acute lymphoblastic leukemia and correlation with the Bruinkins-Oseretsky Test of Motor Proficiency Second Edition Objectives: The aim of this work was to characterize the neurological consequences of vincristine-induced peripheral neuropathy (VIPN) clinically and electromyographically and to evaluate motor skills of pediatric patients after the end of treatment of acute lymphoblastic leukemia. We also determined the relationship between the results of the clinical and electromyographic evaluation of VIPN and the correlation with the results of motor skills tests. Methods: The study involved 35 probands (19 girls and 16 boys) with a mean age of 10.7 years (SD ± 4.3) and a mean time since the last dose of vincristine of 2.3 years (SD ± 1.2). VIPN was assessed using a clinical pediatric-modified Total Neuropathy Score (ped-mTNS) and nerve conduction studies (NCS). Motor skills were assessed using the Bruinkins-Oseretsky Test of Motor Proficiency, Second Edition (BOT-2). Results: The clinical presence of VIPN, according to ped-mTNS, was found in 20 % of probands. Abnormalities in nerve conduction studies were reported by 60.9 % of probands. Of these, 92.9 % had motor...

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Ma, Xiya. "La formation de synapses par les neurones périphériques sur des surfaces synthétiques". Thèse, 2018. http://hdl.handle.net/1866/22316.

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