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Sensorimotor - Science topic

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Hello!
I have a repeated measure dataset, where all subjects were scanned twice (i.e., pre & post) with an interval of 7 days between scans by fMRI. After analyzing by FSL standard pipeline, I got very weird group-level results using insular as ROI.
Pre: the functional connectivity between insular and S1 is Bilateral NEGATIVE!!! (with a large number of voxels) Post: the functional connectivity between insular and S1 is positive (with a small number of voxels) And paired t-test (Post > Pre) found large areas of difference in the sensorimotor region.
This result seems very strange to me as previous research has suggested that the test-retest reliability of resting-state functional connectivity is quite high. However, I am still unclear as to why the sensorimotor region appears to have a negative correlation during the pre-test.
Do any experts have any suggestions on this result? Are there any additional pre-processing methods such as denoising or motion correction that could improve the results?
Many Thanks!!!
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Hi,
Unexpected correlations between the insular and S1 regions could arise from factors like motion artifacts, physiological noise, or inaccuracies in region-of-interest definition. Group-level statistical analysis needs to be robust, ensuring outliers aren't skewing results. Also, the state of subjects during scans, like falling asleep, can impact results. Ensuring accuracy in each step can shed light on these unusual findings.
Hope this helps.
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Rupture of the anterior cruciate ligament (ACL) is the most common traumatic knee injury in active adults. ACL tears (ACLt) tend to occur during activities including sudden acceleration and deceleration, rapid changes of direction, jumping and landing tasks, where rapid and unanticipated movement responses of the medial and lateral hamstring muscles are necessary to stabilize the knee joint and successfully counteract the extreme load forces generated (McLean et al. 2010; Smith et al. 2012). During these movements, numerous muscle actions occur with differing co-contraction strategies required to stabalize the joint.
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Sensorimotor rehabilitation includes rehab tools targeting neural and muscular components. It may include electrotherapy, manual therapy, and strenghening regimes. Balance, coordination, and muscle performance are three different things, requiring different therapeutic protocols. In Hungary, rehabilitation after ACLt is a 4 months managment program, that includes various different protocols; starting from low impact exercises to high impact balance training. The asked question need to be specified with more clarity to have a more specific answer.
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Biological behaviors require intricate coordination between different components, including sensorimotor pathways, muscle groups, and the skeleton. Some of the behaviors for a specific organism can be identified. If their locomotion patterns are in a state-dependent manner, it might be suitable to utilize the Markov model to simulate it. I am wondering what is worth noting during the Markov modeling for locomotion.
And is there any other ideas for the modeling of biological movements?
Thanks for your potential advice in advance.
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Suresh Babu Thanks so much for your kind suggestions. I shall check the relevant papers.
As for the modeling strategies for locomotion patterns, do you have any good advice alternatively?
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This is more a personal question than one related directly to my research (although i am interested in sensorimotor rehabilitation in general). I have a family member who has hemiplegia because of a stroke, and they are considering stem cell treatment offered by a private clinic in Asia. Can autologous stem cells (harvested from one's own fat cells and blood) injected intramuscularly find its way to the brain to repair damaged cortical areas? The doctors who have performed the stem cell therapy (and who claim to have seen significant improvements in some of their patients) tell me three things:
1) Stem cells are automatically attracted to cytokines that signal areas in the body that need repair;
2) These stem cells can be effective even when injected intramuscularly and not intravenously or directly at the site of damage, because cytokines guide the stem cells where they need to go;
3) These stem cells can penetrate the blood-brain barrier.
How true are these claims? I've been looking up research and opinion pieces online already, but I'm expanding my search strategy to include RG. This is what I'm looking at:
Aleynik, A., Gernavage, K. M., Mourad, Y. S., Sherman, L. S., Liu, K., Gubenko, Y. A., & Rameshwar, P. (2014). Stem cell delivery of therapies for brain disorders. Clinical and Translational Medicine, 3, 24. https://doi.org/10.1186/2001-1326-3-24 Bai, L., Lennon, D. P., Caplan, A. I., DeChant, A., Hecker, J., Kranso, J., … Miller, R. H. (2012). Hepatocyte growth factor mediates MSCs stimulated functional recovery in animal models of MS. Nature Neuroscience, 15(6), 862–870. https://doi.org/10.1038/nn.3109 Banerjee, S., Bentley, P., Hamady, M., Marley, S., Davis, J., Shlebak, A., … Chataway, J. (2014). Intra-Arterial Immunoselected CD34+ Stem Cells for Acute Ischemic Stroke. STEM CELLS Translational Medicine, 3(11), 1322–1330. https://doi.org/10.5966/sctm.2013-0178 Berkowitz, A. L., Miller, M. B., Mir, S. A., Cagney, D., Chavakula, V., Guleria, I., … Chi, J. H. (2016). Glioproliferative Lesion of the Spinal Cord as a Complication of “Stem-Cell Tourism.” New England Journal of Medicine, 375(2), 196–198. https://doi.org/10.1056/NEJMc1600188 Gross, G., & Häupl, T. (Eds.). (2013). Stem cell-dependent therapies: mesenchymal stem cells in chronic inflammatory disorders. Berlin: De Gruyter. Harris, V. K., Yan, Q. J., Vyshkina, T., Sahabi, S., Liu, X., & Sadiq, S. A. (2012). Clinical and pathological effects of intrathecal injection of mesenchymal stem cell-derived neural progenitors in an experimental model of multiple sclerosis. Journal of the Neurological Sciences, 313(1–2), 167–177. https://doi.org/10.1016/j.jns.2011.08.036 Hess, D. C., Wechsler, L. R., Clark, W. M., Savitz, S. I., Ford, G. A., Chiu, D., … Mays, R. W. (2017). Safety and efficacy of multipotent adult progenitor cells in acute ischaemic stroke (MASTERS): a randomised, double-blind, placebo-controlled, phase 2 trial. The Lancet Neurology, 16(5), 360–368. https://doi.org/10.1016/S1474-4422(17)30046-7 Liu, L., Eckert, M. A., Riazifar, H., Kang, D.-K., Agalliu, D., & Zhao, W. (2013). From Blood to the Brain: Can Systemically Transplanted Mesenchymal Stem Cells Cross the Blood-Brain Barrier? Stem Cells International, 2013. https://doi.org/10.1155/2013/435093 Steinberg, G. K., Kondziolka, D., Wechsler, L. R., Lunsford, L. D., Coburn, M. L., Billigen, J. B., … Schwartz, N. E. (2016). Clinical Outcomes of Transplanted Modified Bone Marrow–Derived Mesenchymal Stem Cells in Stroke: A Phase 1/2a Study. Stroke, STROKEAHA.116.012995. https://doi.org/10.1161/STROKEAHA.116.012995 Turner, L., & Knoepfler, P. (2016). Selling Stem Cells in the USA: Assessing the Direct-to-Consumer Industry. Cell Stem Cell, 19(2), 154–157. https://doi.org/10.1016/j.stem.2016.06.007 Webb, R. L., Kaiser, E. E., Scoville, S. L., Thompson, T. A., Fatima, S., Pandya, C., … Stice, S. L. (2017). Human Neural Stem Cell Extracellular Vesicles Improve Tissue and Functional Recovery in the Murine Thromboembolic Stroke Model. Translational Stroke Research, 1–10. https://doi.org/10.1007/s12975-017-0599-2
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Hi, the Blood brain barrier(BBB) makes it therapeutically challenging if not impossible to treat neurological disorders. Cells are huge compared to many of the small molecules that the BBB filters out. It is a challenge in such treatments.
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Hi,
I would be thankful for any piece of literature introducing short, accessible and uncomputerised psychological tests for executive functioning and visual-motor processing. I am most interested in assessment of spatial and hierarchical planning.
Thank you
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Stephen, thank you for the reply. I didn't correctly express myself and have now corrected the question. I am not interested in one test which would merge all the functions but in all the tests available which cover the mentioned (not all in one test).
I am familiar with the Tower of Hanoi and I saw that the set can be bought online for a reasonable price, but was still hoping that other planning assessment tasks would be available.
Thank you for suggesting the Porteus Maze test, I will look into it.
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One could argue that a much more empirical set of data, based on concrete and directly observable overt behavior patterns, detectable with eye-tracking technology, at key times, yet in "real time" (i.e. in then-current behavior patterns), could be used, AND HYPOTHESES DIRECTLY TESTED, as explanations for concept development. Start at the following Question:
The "sensori-motor" explanations have turned out as not well-founded and based on VERY indirect evidence, at best, and seen IN PEER REVIEW, as having "no future":
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Thank you for your suggestions regarding the use of eye movements. However, I strongly disagree with your assertion that the embodiment/grounded cognition perspective is unproven and unjustified. You just have a look at several review or original papers demonstrating direct evidence for the role of the sensory-motor system in conceptual cognition. Hence, embodied/grounded cognition theories are clearly supported by sound empirical evidence. Just to mention a few examples:
Kiefer, M., & Pulvermüller, F. (2012). Conceptual representations in mind and brain: Theoretical developments, current evidence and future directions. Cortex, 48, 805-825.
Pulvermüller, F., & Fadiga, L. (2010). Active perception: Sensorimotor circuits as a cortical basis for language. Nature Reviews Neuroscience, 11, 351-360.
Shebani, Z., & Pulvermüller, F. (2013). Moving the hands and feet specifically impairs working memory for arm- and leg-related action words. Cortex, 49, 222-231.
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I am interested in assessing "mania-like behaviors", mainly sensorimotor gating & hyperactivity in both a rat & mouse model. If anyone has an alternative mood stabilizer they prefer (e.g. valproate) for such models, please share your experiences.
TIA!
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I looked over your summary for a cell-free isolated head viability model, and I recall a few issues. How might you account for infection, especially if lymph nodes and bone marrow stem cells have been substantially increased? Likewise, ECMO circulation in hospitals today kills half the patients it's hooked up to, and results in neurological damage on the rest. Also, cutting the spine results in neurological atrophy and degeneration up to the sensorimotor cortex.
I believe that each of these issues is surmountable, but blood and bone marrow are big ones. ECMO can be improved by use of an adapted blood pump and respirator/artificial lung, controlled in a similar way to the vagus nerve. Likewise, neurostimulation via a biocompatible implant (e.g., carbon nanotube-based microelectrode array) could forestall the degeneration and interface directly with neuroprosthetics. What are your thoughts?
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There are queries,there are obvious possible complications into this one undone task. The questions are the most to sort out the answers. Thanks and regards for the same. ECMO is just explained as one of the possible ways to ventilate while artificial lungs are already in clinical trial. Once the complete model will be under development,we will sort out the best possible/developed and verified means to be used instead of those major body parts described. Not only the artificial lungs, we can also consider other means of oxygenating and removal of CO2. And thanks for your idea behind the nerve stimulation to prevent further atrophy. The discussions regarding the pros and cons of every single separate procedures are the most to begin with it. Hope for the continued discussions.
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I'm quite interested in sensorimotor synchronization. If I'm gonna do such an experiment, do I need to make the hardware and software myself or with some engineers? Then questions come out. What is the time error of this measurement system? How to ensure that error in the ideal range?
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Please, give some details of Your experiment. What kind of task do You plan to use? What kind of motion do You want to register?
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I would like to implement the approximated surface Laplacian (SL) estimated using Hjorth Algorithm but I can't find an open literature on the approximation of The SL at scalp edges as suggested in "Spatial Filter Selection for EEG Based Communication" by McFarland et al.
They mention Zhou's work for edge electrodes SL approximation but I do not have access to that literature.
Does anyone have relevant literature on that?
Or Does anyone Know How To Compute The Large Laplacian also called" next nearest neighbor SL" (up to the edge of the scalp)?
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Hi Yves,
you might want to check out the (open-source) implementation in the FieldTrip Matlab toolbox:
In FieldTrip, Hjorth's method is implemented within the function ft_scalpcurrentdensity, see: http://www.fieldtriptoolbox.org/reference/ft_scalpcurrentdensity
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Previous resarch show that these two COP variables can be are tightly dependents, however I would like to know whether there will be a high co-relation in dynamic analysis conditions (i.e, during the unipodal stance, or in the different support, surface or in the sensorimotor constraints).
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The best explanation I have seen regarding the difference between COP and COM is by David Winter in his classic text Biomechanics and Motor Control of Human Movement.
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I am working on Brain Computer Interface and would like to ask the scientific community if there is an existing mathematical model that can simulate neural adatation of the brain more importantly for application in Sensorimotor rythms based Brain Computer Interface.
Your Input will be of great help.
Thanks.
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Yves, this paper might be useful to you:
Eliasmith et al (2012) "A Large-Scale Model of the Functioning Brain"
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Whereas, for the overwhelming majority of persons*, the acquisition of finely detailed visual, aural, tactile, gustatory or olfactory perceptual imagery requires focused attention to a stimulus' features, often repeatedly over an extended period, and for novel features, a degree of purposeful interaction with the stimuli concerned, the acquisition of kinaesthetic (sensorimotor) imagery apparently ensues automatically as the mere consequence of repeated movement-making, without requiring any attention to the qualities of proprioceptive feedback entailed thereby. Furthermore, for the majority, both visual and auditory stimulus-driven percepts, and recalled perceptual imagery, spontaneously evokes context-associated kinaesthetic imagery, whereas recalling that same kinaesthetic imagery typically fails to evoke any specific visual or auditory imagery.
[* Addendum: Explicitly, the majority of persons drawn at random from the general population, who, in their normal course of engaging in purposeful activities,  tend not  to habitually make deliberate reference to any kind of mental imagery for preparing their physical actions.]
Although the above dissimilarites are readily verifiable for oneself and, to my thinking, pinpoint phenomena of importance to theoretical cognitive science, with implications for remedial therapies and training in domains reliant upon perceptual-motor skills, I am not currently aware of research that has specifically investigated these associations and disassociations or pondered the neural substrates differentiating kinaesthetic representation and that of other sensory modalites. For instance, has it been demonstrated that acquisition of kinaesthetic imagery is dependent upon motor-acts being goal-driven and orientated?
I am wondering, does my question summon to anybody's mind somesuch research, and equally interesting from my standpoint, spark off readers' original thoughts on its substance?
In keenest anticipation,
Richard Traub
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The continuum of sensory neural motor systems can function passively or actively. A person is constantly engaged in passive reception of a flood of sensory input; what is attended to is a matter of choice or prioritized for attention by the systems themselves. People develop preferred pathways for processing information probably based on how well it works for them. All sensory input is integrated into memory and when accessed via one sense other senses are recalled. The smell of burnt toast may bring back a memory from childhood walking up a sidewalk and all the other sensory input at the time. I am fascinated by Klaus Blishke inclusion of sports and musical performance. I taught a martial art for 30 years and actively attended to mirror neuron input for learning the art and for fighting. I taught students to practice in their imagination during meditation when actual physical practice was impractical. I based this method on an Olympic high jumper who did the same before his actually attempts. It worked quite well.
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I am looking for a reference with a list of all of the known cortices. I'd like to include reference to all of the six layers, if possible.
For example, Google Scholar has helped me find that smell and taste are associated with O1, O2, G1 G2. The visual cortex has V1, V2, V3, V4, V5/MT, V6. The aural cortex has AI and AII.
Already I am confused. Some of the cortices have fewer than six layers.
When it comes to tactile, proprioceptive, vestibular and sensorimotor effects, I cannot find any associated cortex.
Any guidance that you can provide, including correcting and improving my question, would be greatly appreciated.
Sincerely,
Mark Frautschi, Ph.D.
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any basic textbook on the organization of the brain is mandatory before asking such fundamental information. Have You heard about brain maps and atlasses or cytoarchitectonics? Start here: www.thehumanbrain.info