Journal articles: 'Disordered Locomotion'

1

Winstein, Carolee J., and Alan Garfinkel. "Qualitative Dynamics of Disordered Human Locomotion." Journal of Motor Behavior 21, no. 4 (December 1989): 373–91. http://dx.doi.org/10.1080/00222895.1989.10735490.

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Holt, Kenneth G., John P. Obusek, and Sergio T. Fonseca. "Constraints on disordered locomotion A dynamical systems perspective on spastic cerebral palsy." Human Movement Science 15, no. 2 (April 1996): 177–202. http://dx.doi.org/10.1016/0167-9457(95)00043-7.

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Payne, Anthony P., Roger G. Sutcliffe, Jacqueline M. Campbell, Glenda Favor, David Russell, Neil K. Bennett, Debbie J. Clarke, et al. "Disordered locomotion in the AS/AGU mutant rat and the effects ofL-dopa or fetal midbrain grafts." Movement Disorders 13, no. 5 (September 1998): 832–34. http://dx.doi.org/10.1002/mds.870130514.

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Asante, Curtis Oware, Amy Chu, Mark Fisher, Leora Benson, Asim Beg, Peter Scheiffele, and John Martin. "Cortical Control of Adaptive Locomotion in Wild-Type Mice and Mutant Mice Lacking the Ephrin-Eph Effector Protein α2-Chimaerin." Journal of Neurophysiology 104, no. 6 (December 2010): 3189–202. http://dx.doi.org/10.1152/jn.00671.2010.

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In voluntary control, supraspinal motor systems select the appropriate response and plan movement mechanics to match task constraints. Spinal circuits translate supraspinal drive into action. We studied the interplay between motor cortex (M1) and spinal circuits during voluntary movements in wild-type (WT) mice and mice lacking the α2-chimaerin gene (Chn1−/−), necessary for ephrinB3-EphA4 signaling. Chn1−/− mice have aberrant bilateral corticospinal systems, aberrant bilateral-projecting spinal interneurons, and disordered voluntary control because they express a hopping gait, which may be akin to mirror movements. We addressed three issues. First, we determined the role of the corticospinal system in adaptive control. We trained mice to step over obstacles during treadmill locomotion. We compared performance before and after bilateral M1 ablation. WT mice adaptively modified their trajectory to step over obstacles, and M1 ablation increased substantially the incidence of errant steps over the obstacle. Chn1−/− mice randomly stepped or hopped during unobstructed locomotion but hopped over the obstacle. Bilateral M1 ablation eliminated this obstacle-dependent hop selection and increased forelimb obstacle contact errors. Second, we characterized the laterality of corticospinal action in Chn1−/− mice using pseudorabies virus retrograde transneuronal transport and intracortical microstimulation. We showed bilateral connections between M1 and forelimb muscles in Chn1−/− and unilateral connections in WT mice. Third, in Chn1−/− mice, we studied adaptive responses before and after unilateral M1 ablation. We identified a more important role for contralateral than ipsilateral M1 in hopping over the obstacle. Our findings suggest an important role for M1 in the mouse in moment-to-moment adaptive control, and further, using Chn1−/− mice, a role in mediating task-dependent selection of mirror-like hopping movements over the obstacle. Our findings also stress the importance of subcortical control during adaptive locomotion because key features of the trajectory remained largely intact after M1 ablation.

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Rizzo-Sierra, Carlos V., Alexander Gonzalez-Castaño, and Fidias E. Leon-Sarmiento. "Galvanic vestibular stimulation: a novel modulatory countermeasure for vestibular-associated movement disorders." Arquivos de Neuro-Psiquiatria 72, no. 1 (January 2014): 72–77. http://dx.doi.org/10.1590/0004-282x20130182.

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Motion sickness or kinetosis is the result of the abnormal neural output originated by visual, proprioceptive and vestibular mismatch, which reverses once the dysfunctional sensory information becomes coherent. The space adaptation syndrome or space sickness relates to motion sickness; it is considered to be due to yaw, pith, and roll coordinates mismatch. Several behavioural and pharmacological measures have been proposed to control these vestibular-associated movement disorders with no success. Galvanic vestibular stimulation has the potential of up-regulating disturbed sensory-motor mismatch originated by kinetosis and space sickness by modulating the GABA-related ion channels neural transmission in the inner ear. It improves the signal-to-noise ratio of the afferent proprioceptive volleys, which would ultimately modulate the motor output restoring the disordered gait, balance and human locomotion due to kinetosis, as well as the spatial disorientation generated by gravity transition.

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Douglas, Christopher L., Grant N. Bowman, Helen A. Baghdoyan, and Ralph Lydic. "C57BL/6J and B6.V-LEPOB mice differ in the cholinergic modulation of sleep and breathing." Journal of Applied Physiology 98, no. 3 (March 2005): 918–29. http://dx.doi.org/10.1152/japplphysiol.00900.2004.

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Respiratory and arousal state control are heritable traits in mice. B6.V-Lepob (ob) mice are leptin deficient and differ from C57BL/6J (B6) mice by a variation in the gene coding for leptin. The ob mouse has morbid obesity and disordered breathing that is homologous to breathing of obese humans. This study tested the hypothesis that microinjecting neostigmine into the pontine reticular nucleus, oral part (PnO), of B6 and ob mice alters sleep and breathing. In B6 and ob mice, neostigmine caused a concentration-dependent increase ( P < 0.0001) in percentage of time spent in a rapid eye movement (REM) sleeplike state (REM-Neo). Relative to saline (control), higher concentrations of neostigmine increased REM-Neo duration and the number of REM-Neo episodes in B6 and ob mice and decreased percent wake, percent non-REM, and latency to onset of REM-Neo ( P < 0.001). In B6 and ob mice, REM sleep enhancement by neostigmine was blocked by atropine. Differences in control amounts of sleep and wakefulness between B6 and the congenic ob mice also were identified. After PnO injection of saline, ob mice spent significantly ( P < 0.05) more time awake and less time in non-REM sleep. B6 mice displayed more ( P < 0.01) baseline locomotor activity than ob mice, and PnO neostigmine decreased locomotion ( P < 0.0001) in B6 and ob mice. Whole body plethysmography showed that PnO neostigmine depressed breathing ( P < 0.001) in B6 and ob mice and caused greater respiratory depression in B6 than ob mice ( P < 0.05). Western blot analysis identified greater ( P < 0.05) expression of M2 muscarinic receptor protein in ob than B6 mice for cortex, midbrain, cerebellum, and pons, but not medulla. Considered together, these data provide the first evidence that pontine cholinergic control of sleep and breathing varies between mice known to differ by a spontaneous mutation in the gene coding for leptin.

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SATO, Keisuke, and Naoto FUKUMURA. "Freight Locomotive Rescheduling Algorithm under Disordered Train Operation." Quarterly Report of RTRI 52, no. 2 (2011): 81–85. http://dx.doi.org/10.2219/rtriqr.52.81.

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Popova-Petrosyan, Elena V., Shanmugaraj Kulanthaivel, and Keerthanaa Balasundaram. "Development of Secondary Osteoporosis in Teenage Girls with Menstrual Disorders." Current Women s Health Reviews 16, no. 1 (January 21, 2020): 26–32. http://dx.doi.org/10.2174/1573404815666190923121305.

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Introduction: Nowadays, the most common problem in teenage girls is them facing menstrual disorders that develop secondary osteoporosis in their adolescent period. The locomotor system disorder is noticed more often in girls with adolescence hormone pathology, than in the population. This has an enormous human and socio-economic impact. Osteoporosis is estimated to affect 200 million women worldwide. Objective: The aim of this research is to determine the development of secondary osteoporosis in girls during their adolescent period. Materials and Methods: An analysis of 173 girls aged from 13 to 17 were under our supervision in the children’s clinic sanatorium “Zdravnisa”. Girls were divided into four groups according to their menstrual disorders. Results: As per the correlation analysis data, the influence of steroid hormones level on bone content has a cumulative effect on girls. Conclusion: For patients with oligomenorrhea, secondary amenorrhea, and polymenorrhea, there were disordered correlations of gonadotropic hormones. Correlations between calcium, phosphorus, and magnesium are disordered, which can be proof of mineralization processes disorder. As per the correlation analysis data for the girls with adolescence pathology, there were revealed direct average correlation connections between the concentration of steroid hormones and structural-functional properties of bony tissue. Low concentration of progesterone in the blood of girls with adolescence pathology is one of the main reasons for bone content deficit, development of osteoporosis, and scoliosis progression.

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Zehr, E. Paul, Pamela M. Loadman, and Sandra R. Hundza. "Neural control of rhythmic arm cycling after stroke." Journal of Neurophysiology 108, no. 3 (August 1, 2012): 891–905. http://dx.doi.org/10.1152/jn.01152.2011.

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Disordered reflex activity and alterations in the neural control of walking have been observed after stroke. In addition to impairments in leg movement that affect locomotor ability after stroke, significant impairments are also seen in the arms. Altered neural control in the upper limb can often lead to altered tone and spasticity resulting in impaired coordination and flexion contractures. We sought to address the extent to which the neural control of movement is disordered after stroke by examining the modulation pattern of cutaneous reflexes in arm muscles during arm cycling. Twenty-five stroke participants who were at least 6 mo postinfarction and clinically stable, performed rhythmic arm cycling while cutaneous reflexes were evoked with trains (5 × 1.0-ms pulses at 300 Hz) of constant-current electrical stimulation to the superficial radial (SR) nerve at the wrist. Both the more (MA) and less affected (LA) arms were stimulated in separate trials. Bilateral electromyography (EMG) activity was recorded from muscles acting at the shoulder, elbow, and wrist. Analysis was conducted on averaged reflexes in 12 equidistant phases of the movement cycle. Phase-modulated cutaneous reflexes were present, but altered, in both MA and LA arms after stroke. Notably, the pattern was “blunted” in the MA arm in stroke compared with control participants. Differences between stroke and control were progressively more evident moving from shoulder to wrist. The results suggest that a reduced pattern of cutaneous reflex modulation persists during rhythmic arm movement after stroke. The overall implication of this result is that the putative spinal contributions to rhythmic human arm movement remain accessible after stroke, which has translational implications for rehabilitation.

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Duval, Karine, Kathryn Luttin, and Tania Lam. "Neuromuscular strategies in the paretic leg during curved walking in individuals post-stroke." Journal of Neurophysiology 106, no. 1 (July 2011): 280–90. http://dx.doi.org/10.1152/jn.00657.2010.

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Reduced flexibility over the neuromotor control of paretic leg muscles may impact the extent to which individuals post-stroke modulate their muscle activity patterns to walk along curved paths. The purpose of this study was to compare lower-limb movements and neuromuscular strategies in the paretic leg of individuals with stroke with age-matched controls during curved walking. Participants walked at their preferred walking velocity along four different paths of increasing curvature, while lower-limb kinematics and muscle activity were recorded. A second group of able-bodied individuals walked along the four paths, matching the walking speed of the stroke group. The stroke group showed reduced lower-limb joint excursion and disordered modulation of foot pressure during curved walking, accompanied by reduced modulation of muscle activity patterns. In the inner leg of the curve in control subjects, the posteromedial muscles (medial gastrocnemius and medial hamstrings) showed decreased electromyographic amplitude as path curviture increased. Conversely, activity of the posterolateral musculature of the outer leg was decreased with increasing path curvature. Activity in the tibialis anterior and gluteus medius was also modulated with path curvature. However, in the stroke group, we found reduced modulation of muscle activity in the paretic leg during curved walking. The extent of modulation was also associated with the level of physical impairment due to stroke. The results of this study provide further knowledge about neuromuscular control of locomotor adaptations post-stroke.

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LINDSAY, LISA A. "‘NO NEED...TO THINK OF HOME’? MASCULINITY AND DOMESTIC LIFE ON THE NIGERIAN RAILWAY, c. 1940–61." Journal of African History 39, no. 3 (November 1998): 439–66. http://dx.doi.org/10.1017/s0021853798007312.

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In 1950, a young man named Ayo Salako went to work for the Nigerian railway as a casual laborer. He hoped to be like his father, a locomotive driver who had worked for the railway from 1916 to his death thirty-four years later. Indeed, Ayo Salako became a successful railwayman, climbing the career ladder to locomotive driver, transferring to a number of different stations and retiring with a pension in 1987. Although the two generations of men both made long, continuous careers in railway employment, Ayo Salako was rather different from his father in terms of his domestic life. The elder Salako had parlayed his employment success into a polygamous marriage and the maintenance of a farm and patron–client relations in his hometown of Ogbomosho. His son, in contrast, married his current wife only after the dissolution of a previous marriage, visited Ogbomosho infrequently and retired in Ibadan rather than in his patrilineal hometown. During his career he saw himself as a modernizer, involved with industrial technology, well-traveled within the country, monogamous, and building a life and educating his children in the booming towns of post-war Nigeria.Ayo Salako's young adulthood during the 1940s and 1950s coincided with important economic, social and political transformations in Nigeria and throughout Africa. The Second World War and the end of the depression brought economic expansion and a new wave of government interventionism. Cities were swollen with migrants looking for cash and the independence from elders that came with it. African railways expanded to meet new demands for transport and their work forces were among the largest and most politically active on the continent. Faced with imperial financial pressures and widespread African dissent, officials were turning to new policies for the colonies. Ambitious planners attempted to rationalize peasant agriculture to increase production, stabilize wage labor to improve efficiency, reshape African cities to make them less ‘disorderly’ and mold African family life to conform more closely to a bourgeois European image.

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12

McGovern, Kathryn E., J. Philip Nance, Clément N. David, Reed E. S. Harrison, Shahani Noor, Danielle Worth, Tyler A. Landrith, et al. "SPARC coordinates extracellular matrix remodeling and efficient recruitment to and migration of antigen-specific T cells in the brain following infection." Scientific Reports 11, no. 1 (February 25, 2021). http://dx.doi.org/10.1038/s41598-021-83952-0.

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AbstractCentral nervous system (CNS) injury and infection can result in profound tissue remodeling in the brain, the mechanism and purpose of which is poorly understood. Infection with the protozoan parasite Toxoplasma gondii causes chronic infection and inflammation in the brain parenchyma. Control of parasite replication requires the continuous presence of IFNγ-producing T cells to keep T. gondii in its slowly replicating cyst form. During infection, a network of extracellular matrix fibers, revealed using multiphoton microscopy, forms in the brain. The origin and composition of these structures are unknown but the fibers have been observed to act as a substrate for migrating T cells. In this study, we show a critical regulator of extracellular matrix (ECM) remodeling, Secreted Protein, Acidic, Rich in Cysteine (SPARC), is upregulated in the brain during the early phases of infection in the frontal cortex. In the absence of SPARC, a reduced and disordered fibrous network, increased parasite burden, and reduced antigen-specific T cell entry into the brain points to a role for SPARC in T cell recruitment to and migration within the brain. We also report SPARC can directly bind to CCR7 ligands CCL19 and CCL21 but not CXCL10, and enhance migration toward a chemokine gradient. Measurement of T cell behavior points to tissue remodeling being important for access of immune cells to the brain and facilitating cellular locomotion. Together, these data identify SPARC as an important regulatory component of immune cell trafficking and access to the inflamed CNS.

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Ho, Rachel Xi-Yeen, Razie Amraei, Kyle Oliver Corcino De La Cena, Evan G. Sutherland, Farzad Mortazavi, Thor Stein, Vipul Chitalia, and Nader Rahimi. "Loss of MINAR2 impairs motor function and causes Parkinson’s disease-like symptoms in mice." Brain Communications 2, no. 1 (January 1, 2020). http://dx.doi.org/10.1093/braincomms/fcaa047.

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Abstract Parkinson’s disease is the second most common human neurodegenerative disease. Motor control impairment represents a key clinical hallmark and primary clinical symptom of the disease, which is further characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of α-synuclein aggregations. We have identified major intrinsically disordered NOTCH2-associated receptor 2 encoded by KIAA1024L, a previously uncharacterized protein that is highly conserved in humans and other species. In this study, we demonstrate that major intrinsically disordered NOTCH2-associated receptor 2 expression is significantly down-regulated in the frontal lobe brain of patients with Lewy body dementia. Major intrinsically disordered NOTCH2-associated receptor 2 is predominantly expressed in brain tissue and is particularly prominent in the midbrain. Major intrinsically disordered NOTCH2-associated receptor 2 interacts with neurogenic locus notch homologue protein 2 and is localized at the endoplasmic reticulum compartments. We generated major intrinsically disordered NOTCH2-associated receptor 2 knockout mouse and demonstrated that the loss of major intrinsically disordered NOTCH2-associated receptor 2 in mouse results in severe motor deficits such as rigidity and bradykinesia, gait abnormalities, reduced spontaneous locomotor and exploratory behaviour, symptoms that are highly similar to those observed in human Parkinson’s spectrum disorders. Analysis of the major intrinsically disordered NOTCH2-associated receptor 2 knockout mice brain revealed significant anomalies in neuronal function and appearance including the loss of tyrosine hydroxylase-positive neurons in the pars compacta, which was accompanied by an up-regulation in α-synuclein protein expression. Taken together, these data demonstrate a previously unknown function for major intrinsically disordered NOTCH2-associated receptor 2 in the pathogenesis of Parkinson’s spectrum disorders.

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Fouad, Mohamed, and Maher Boraie. "The Impact of Chronic Kidney Disease - Mineral and Bone Disorder on the Locomotor System and Quality of Life in Hemodialysis Patients." Turkish Nephrology Dialysis Transplantation 24, no. 3 (September 18, 2015). http://dx.doi.org/10.5262/tndt.2015.1003.08.

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15

Li, Xiao-Hong, Xiang Zhu, Xiao-Yin Liu, Hai-Huan Xu, Wei Jiang, Jing-Jing Wang, Feng Chen, et al. "The corticospinal tract structure of collagen/silk fibroin scaffold implants using 3D printing promotes functional recovery after complete spinal cord transection in rats." Journal of Materials Science: Materials in Medicine 32, no. 4 (March 22, 2021). http://dx.doi.org/10.1007/s10856-021-06500-2.

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AbstractNo effective treatment has been established for nerve dysfunction caused by spinal cord injury (SCI). Orderly axonal growth at the site of spinal cord transection and creation of an appropriate biological microenvironment are important for functional recovery. To axially guiding axonal growth, designing a collagen/silk fibroin scaffold fabricated with 3D printing technology (3D-C/SF) emulated the corticospinal tract. The normal collagen/silk fibroin scaffold with freeze-drying technology (C/SF) or 3D-C/SF scaffold were implanted into rats with completely transected SCI to evaluate its effect on nerve repair during an 8-week observation period. Electrophysiological analysis and locomotor performance showed that the 3D-C/SF implants contributed to significant improvements in the neurogolical function of rats compared to C/SF group. By magnetic resonance imaging, 3D-C/SF implants promoted a striking degree of axonal regeneration and connection between the proximal and distal SCI sites. Compared with C/SF group, rats with 3D-C/SF scaffold exhibited fewer lesions and disordered structures in histological analysis and more GAP43-positive profiles at the lesion site. The above results indicated that the corticospinal tract structure of 3D printing collagen/silk fibroin scaffold improved axonal regeneration and promoted orderly connections within the neural network, which could provided a promising and innovative approach for tissue repair after SCI.

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Journal articles on the topic 'Disordered Locomotion'

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