Questions related to Spinal Cord Injury
I want to cite a clinical trial from clinicaltrial.gov of incertin mimetic exenatide in spinal cord injury. However i am unable to get the citation of the study. I also tried google Scholar searching the heading of the study but with no success. Please let me know how can I cite this study using endnote
Hello, we applied Epidural Electrical Stimulation to a patient who had a Spinal Cord Injury for the first time in Turkey. As a result of my literature research, no information was given about the design of rehabilitation programs. How should the rehabilitation program be shaped for this patient? Also, how should epidural electrical stimulation mapping be?
We hope to commence a study to develop a local rehabilitation guidelines for individuals who suffer spinal cord injury. However, to accomplish that we shall be glad to receive contributions from experts who have done some works in this area. We are also open to collaboration, however, we do not have funding as at present.
I will develop materials for the repair of nerve damages in my master thesis, and I am planning to use neural cells for cell culture experiments. I have cell culture knowledge, but I have never worked with any kind of neural cells. If you have experience on this subject, can you tell me which cell line would be more proper and easy to handle for me and what should be considered differently from basic cell culture in this process?
In the article - Pressure distribution analysis in three wheelchairs cushions of subjects with spinal cord injury. I know the brand names of the cushions but I was wondering if you could let e know what the specific model of each cushion was so I can exclude or include it in a literature search. I am looking into high specification foam cushions and I wondered if these were HSFC or whether they were active cushions - I know the Roho will be an aircell cushion but I wasn't sure about the other two.
Thank you, Sarah
I tried to perform SSEP test in rat SCI model but I had the problems in anesthesia. I used the thiopental (that we had in lab.) 30 mg/kg IP, but the rats hadn't good anesthesia or died.
What is the suitable method to anesthesia in somatosensory evoked potential test in rat spinal cord injury model?
i am working on a Spinal Cord Injury Model and in order to characterize the lesion I want to do a 3 D Reconstruction of a spinal cord. Therefore, I have cut a Spinal cord of 1 cm into 10 µm sections; 4 cuts on one slide.
I Have tried FIJI but i am not happy with it. I need a 3D Reconstruction with which I can interact and measure Volume trauma in the reconstruction.
Does anyone know how to solve this problem?
Every help is very much appreciated.
I'm having trouble with the high mortality rate of my zebrafish after surgery. ( the surgery is done based on this article:
Becker, C. G., Lieberoth, B. C., Morellini, F., Feldner, J., Becker, T., & Schachner, M. (2004). L1. 1 is involved in spinal cord regeneration in adult zebrafish. Journal of Neuroscience, 24(36), 7837-7842. Chicago)
They die in a day or less after surgery. Has anybody got experience with that? after surgery, they are maintained separately in aging water (28 ° C)in dark with no food.
I would like to collect the cervical spinal cord sample from rat following retrograde tracer injection in the forelimb muscles. After collecting the sample, I would like to find out the corticospinal tract changes. Can anyone please help me to find out a protocol for IHC and 3D-Z.1light-sheet microscopical view of the cervical spinal cord.
Thanks in advance.
When treating patients with abnormal tone, I often find recurrent inhibition using a range of sensory modalities from cooling to electrical stimulation at low levels is very effective in some patients. Others respond best to reciprocal activity. Clearly, spasticity results from an inbalance of inhibitory and excitatory activity, but can we deduct or identify which? If so, does that have a direct influence on central or peripheral management of tone? While Botox and other end organ interventions work, I am looking for ways to alter the central activity related to the abnormal tone.
I am trying to couple angiogenesis and osteogenesis in a rodent model of spinal cord injury. What I would like to do is take a bone which exhibits osteoporosis (bone loss) and couple this with the absence of type H vessels by staining for CD31 and Endomucin.
Is it possible to fix a bone in formalin, then microCT scan it the next day, and then decalcify the same bone and perform IHC / histology on it without compromising results?
Also, are there any better stains you would recommend to analyse bone vasculature?
Disabled people are considered under WHO recommandations for daily physical activity, but standard measures used for healthy people could them really be used at the same for disabled ?
In other way, for example, for a femoral amputee, walking at 4m/s speed is it under 3 MET (very low level activity) or over (low activity)?
Autonomic dysreflexia (AD) is a life-threatening condition. AD is more frequently reported among SCI patients with higher lesions (e.g. cervical lesions). How about patients with lower lesions?
I did my research project on the assumption that the neuroma would somehow be influenced by the presence or absence of the communicating branch. My sample was only 40 cadavers, but there was no apparent link that we found in that sample group. I would be very interested in pursuing this further.
I am considering using the EQ-5D-5L instrument (https://euroqol.org/wp-content/uploads/2016/09/EQ-5D-5L_UserGuide_2015.pdf) in people with spinal cord injury. The mobility item of the scale asks about the ability of the person to "walk about". Would anybody know if there is an adapted version for people using a wheelchair? Something that would potentially use the word "mobiling" or "moving from A to B" instead of "walking about"?
I would appreciate any guidance on this.
Recently, i'd gone through an article of Clinical Biomechanics titled "Mechanomyography responses characterize altered muscle function during electrical stimulation-evoked cycling in individuals with spinal cord injury".
On page 24 (page 4 of the article), section 2.7 Data Analysis, line 3 to 7, it was mentioned "...were normalized to their respective peak values considering all the participants and trials....".
It seems the authors took the maximum value in the PRE condition from all the 6 subjects, and normalize the other data w.r.t that peak value. If someone can confirm whether the authors normalized each subject w.r.t that subject's peak value OR they took one peak value for all subjects and normalize all w.r.t that highest among all subjects peak value?
Is it really possible, i.e. to normalize w.r.t a single value for the whole experiment over different subjects?
- One of my concerns is the limitations available for people with disabilities, especially those with spinal cord injury and I want to help them.
- My idea is to send brain orders to the organs via "WiFi", for this purpose a transmitter chip is embedded in the brain and a receiver chip also after the spinal cord injured.
- Is it possible? What problems will there be for the implementation of this idea?
i'm working on a spinal cord injury model. Basicall, I drilled a hole in the left hemisphere of spinal cord. Though this leads to a paralysis of the corresponding parts, many mice died in the first week or two. Does anyone have any ideas about what happened? What did I mess up?
We are recording muscle spasticity in rats after spinal cord injury when stimulation is applied. While recording, we see that there is more deflection in one direction (either positive or negative depending on the arrangement of the electrodes themselves) than the other. Just looking for any possible causes and solutions. I attached an example of this uneven deflection.
I added a picture of our current setup. For the recording and ground electrodes, we are using patch electrodes that only make contact with the surface of the tail. The red and white clamps are the recording and the black is the ground. The stimulating electrode we are using is a cuff style electrode. This is the yellow electrode seen closer to the tip of the tail. We are acquiring the patch electrodes from Biopac, the same company that produces the clamps that the electrodes attach to and the hardware we are using to record and shock with. The stimulating electrode is made in our lab. It is made from 1/8 inch inner diameter tygon tubing that has silver wire threaded through that has been soldered to a conducting wire. The patch electrodes already come with adhesive on them but we use velcro cable ties to ensure that the electrodes are making contact with the tail. We have tried altering the placement of the clamps on the electrodes but nothing seems to eliminate the uneven deflection.
Because of gliosis injured axons unable to regenerate which has become a crucial target for regeneration research in Spinal Cord Injury O(SCI). So, I want to know research specific mechanism. If, possible please give me an illustration of it.
After SCI, glial scarring by astrocytes inhibit axon regeneration. So, which intracellular components induce glial scar?
For people with central nervous system disorders, how much joint assistance or individual's effort is required for joint movement to restore motor function or better motor learning? What factor that defines The optimum assistance for reorganization of CNS is? Please tell me the papers or information on these.
Thank you for your reply in advance,
I've been having a trouble that rats were dying during contusive spinal cord injury.
When I make a contusive injury model, rats should be anesthetized with katamine(90mg/kg) and xylazine(5mg/kg), then laminectomy at the 10th thoracic vertebra.
As you well know, before laminectomy, the lesion site should be incised of skin with blade then removed fat tissue. There has been happened in next step.
To detach of the muscle from bone on the spinal laminae, retractors are positioned to keep the incision widely open, in this the procedure,
the rats suddenly stopped breathing and be die after a couple seconds.
There was no bleeding. and specific problem during surgery, I guess something give a vital problem to rats to breath.
I don`t know what is the problem, I thought the problem might anesthetize, but even though the concentration of ketamine was increased, the problem was happend..
Anyone have a experience that the animals during surgery can not breath suddenly?
Hello!does anyone have experience with glycerol-induced muscle injury?I I have to assess the in vivo differentiation capability of my stem cells but I did not find any remark about the reference of glycerol used. I just need the reference to order it. Thank you!
In BrainQ, I've developed a therapeutic device that have shown to increase rehabilitation process in animal model after stroke, SCI, and TBI, where the major phenomena was to regenerate white matter of specific neural networks that lead to re-gaining lost functions. However, one of the main questions is the rate of degeneration of axons after stroke. In our paper we can see that after stroke, 2 weeks later to the stroke, the rat (stroke side) CC is invisible in the MRI/DTI image. I be be grateful to hear your opinion on this mater, which reflect on treatment of people after stroke.
with reference to various research articles; relating to various spinal cord injury experiments, the spinal cord is preferred to be harvested from live animal (mouse, dog) for the purpose of western blotting and immuno cytochemistry, but circumstances are not every time favorable to collect the spinal cord from live animal. do the livability of animal affect the integrity of spinal cord? can it be harvested while the animal is dead during experimental period?
i need to know the significance of spinal cord harvesting from live animal.
I have control rats that developed mechanical hypersensitivity over time that is comparable to my experimental rats (streptozotocin induced DM).
What filaments do female/male control/naive sprague dawley rats usually respond to and when does repetitive testing start to influence withdrawal thresholds, as described by Chaplan (J. Neurosci. Meth. 1994 53: 55-63)?
Does anyone know of literature that supports the influence of anything other than an induced model (nerve injury, experimental diabetes, spinal cord injury etc) on withdrawal responses in rats?
I am a student occuaptional therapy and I am writing a thesis about the the interventions that can be used in therapy for patients with hand injuries because of spinal cord injury.
So I am searching for literature that gives the link between upper limb and hand rehabilitation after SCI and occupational therapy.
All suggestions about literature about this topic are welcome.
Thank you for your attention!
What protocols training respiratory muscles used for patients with spinal cord injury?
I continue or interval training?
What training loads used?
I read that syrinx formation may be associated with pain that develops after a year or so? What all the factors that may lead to syrinx formation in SCI? Is over-exercise a reason for that?
Which model is best to start with? We are going to start up a SCI model, and also have seen that weight drop model outnumbers the baloon compression model at pubmed. Please advice what is the end point differece between these too.
your advice's will be highly appreciated.
Abdominal viszeral pain is an increasing problem in patients with neurogenic bowel desease after spinal cord injury. We try alwas to improve bowel function. But especially in patients with higher spinal cord lesions the pain remains. What is to do?
Hi, we work in a acute neurorehabilitation clinic admitting SCIs in the first 8 weeks of the injury onset and we have difficulties with the tetraplegic patients during upright positioning trials. Nonpharmachologic(ie: corset,pneumotic compression, fluid intake, meal, urinary and GI tract precautions) and pharmachologic (ie: midodrine up to 30mg) management strategies usually do not work in the first months. For example many patients do not tolerate upright positioning although they can be positioned 60 degree on the tilt table for 15-20 minutes or ortostatic hypotension problems do not resolve in complete tetraplegics up to 4-6 months. Can anyone have experience about ideal timing for upright positioning of tetraplegics and ideal pharmachologic (forexample fluidrocortisone?) treament strategies for ortostatic hypotension during the acute phase rehabilitation process?
Very often I'm working with people that are impaired by a traumatic spinal cord injury. People elaborate this loss along some more-or-less-defined phases, that are very alike to the phases of grief.
Usually the period of grief ends with the possibility, for the person, to put his/her resources on new objectives.
However in the case of acquired disabilities the entity of the loss is enormous and may impair each future scenario.
Are there studies, based on a cognitive - behavioural framework, that may help me to better understand how to face these problems?
I am a student who is writing a thesis about the link between upper limb and hand rehabilitation after SCI and occupational therapy.
All suggestions about literature about this topic are very welcome!
Does anybody have some reference about this subject ?
Especially, I don't know if there's something about difference between paraplegic and tetraplegic patients, even if they're lying on a bed 24 hours a day to heel a pressure ulcer.
i really confused about where is the best place to put the electrode for rehabilitation of hand, which the place for each muscle in hand is complex and have specific movement each. Example, to make circular wrist movement or extension and flexion elbow joint.
I wondered wheter it is possible to merge axial and sagittal T2w images of spinal cord lesions (same field of view) into one image. Does anyone know a software which has a pipeline included?
As you know the scar in the SCI patients and animal models forms inside the spinal cord tissue and forms a cavity but there are a lot of investigations that applied electrospinning nanofibers for motor neuron recovery and astroglioal scar decrement. I think the sheets of electrospinning nanofiber just affects through mechanotransduction pathways and its effects is not direct and maybe hydrogel based scaffold is a true option instead of it. Electrospinning nanofiber is a good option for peripheral nerve regeneration not SCI. What is your opinion about it?
The Trial & Error Prize is seeking spinal cord injury data so that the research community can learn from each other and not duplicate experiments.
In this round of the Prize, there will be a total prize fund of $6,000 available, with up to $3,000 available for the top application.
The application deadline is January 21st 2016, and we welcome all interest and any questions. To view and enter the grants, please go to http://www.conquerparalysisnow.org/RibbonLinks/TEPrize/Overview.aspx
I need to analyze the fibrotic scar size in a mouse model of spinal cord injury and i used laminin-specific antibody,but it didn't work well.
Can anyone suggest a good antibody?
if the fibroblast migration is arrested after spinal cord injury immediatelly by using some kind of drug such as taxol, will it migrate again toward the lesion site at the chronic stage after the drug delivery is stopped?
because i think the inflammatory molecules will be reduced at the chronic stage, if the inflammatory molecules are the reason that cause fibrosis, inhibition of fibroblast migration at the acute stage is enough to reduce the fibrotic scar and the fibrotic scar will not occur at the chronic phase,am i right?
Can we adapt the strategies in brain injured patients?
In a recent pilot study, Werndle et al. presented preliminary data of a new technique for the continuous monitoring of spinal cord pressure and the corresponding spinal cord perfusion pressure (Crit Care Med 2014;42:646–655). Their analyses revealed that the use of inotropic drugs for an increase of spinal cord perfusion pressure optimizes neuronal function measured by motoric evoked potentials and muscle strengths below the spinal level of injury.
Are we ready for a routinely monitored management of spinal cord perfusion?
Which mean arterial blood pressure should be targeted in this context?
How long and how invasive should we monitor?
We want to evaluate temproal changes in the bladder function of rats with a spinal cord injury. In order to minimize costs we would like to have a clinical outcome measure, so we wonder if there are valid clinical tests to assess bladder function in rats.
The SRS scores reported in scoliosis series are highly variable. Some authors use SRS22, others SRS30. Some papers report SRS as mean for each domain, and others report a total score. How can I convert these scores into a single one in order to do a meta-analysis? Do you have any reference?
Alisson R. Teles
Is there a policy on early enteral feeding or is it a wait-and-see approach dependent on adequate oral intake? What factors influence the decision to transition from an nasogastric tube to a gastrostomy? Are patients involved in this decision making process?
I have been struggling lately with a rather peculiar problem with immunohistochemistry. My project entails transplantation of stem cells (engineered with an MSCV retrovirus), into a lesion model of spinal cord injury. I am seeing alot of "unspecific background" in the lesion animals in both fluorescence and DAB labeling due to the nature of performing IHC on injured tissue, this I have been able to control with appropriate blocking and treating of the tissue so unspecific binding is not my problem.
What remains a problem that is completely different from "unspecific background", is the fact that I am seeing highly "specific" antibody staining of secondary antibody controls only in animals that A) received a lesion, and B) also received stem cells. Again, to reword, I have used transplant tissue as a secondary control and am seeing very specific cytoplasmic staining of only secondary antibodies that are made against mouse (Gt x Ms IgG). This problem does not exist with secondary antibodies made in other species. This remains a problem because our lab works on a system that uses predominately Ms and Rb primary antibodies, and many of the antibodies I need to use are made in Ms with almost no other option for buying IHC compatible antibodies in other species (e.g. IBA-1 or CD11b are almost exclusively made in mouse, or are not compatible with IHC when made in other species, if anyone can suggest a good substitute that would help alot too). More specifics of my protocols are the following. 4% PFA transcardial perfusion with overnight post-fixation, 25 micron sectioning, wash/ Peroxidase, avidin and biotin blocking if necessary/10% NGS/primary overnight/ 3x wash/ secondary 1 hour/ abc amplification and DAB development if necessary (main problem is in fluorescence).
To clarify species interactions, I use rat models and rat stem cells, but the problem appears localized to stem cell treated animals, ms secondary antibodies, and to regions within the needle track/ lesion epicenter making me think it is something going on with the transplanted cells. This problem does not exist in ICC cover-slipped stem cells, just transplanted ones. As one could imagine it remains impossible to make logically sound conclusions when this is a confounding variable. Please help if you know a solution or have experienced similar problems. I have exhausted alot of testing and controls into figuring this out and have stumped everyone else I have sought out help from.
Update: I know this question is many years old but the problem was, as Jan Johnson stated, Fc receptors present on some kind of inflammatory cell that reacted to the transplanted stem cells. If not Fc receptors, than something similar that arises in response to adaptive immunity, that rejected the transplanted cells.
The Trial & Error Prize aims to incentivise the publication of ‘negative’ results, using crowdvoting and ResearchGate's open review system . Through this Prize, we hope to propel innovation in spinal cord injury (SCI) research through collaboration and information sharing.
The Trial & Error Prize is part of the ground-breaking CPN Challenge Program which will give up to $10 million in prizes and grants over the next 10 years for those who can provide significant improvements in the quality of life of people living with spinal cord injury. To increase the success of this Challenge, we believe that it is important to create a community whereby people can share their experiences and past research that might not have been successful as they hoped; researchers can learn from each other and thus narrow down pathways of innovation.
We currently have $3,000 available for our first round of prizes and the deadline is June 1st 2015.You can find out further information on how to enter please go to http://conquerparalysisnow.org/RibbonLinks/TrialandError/Overview.aspx.
I have attached a useful infographic outlining the prize. If you have any queries, please do not hesitate to email firstname.lastname@example.org.
Patients and families can find BID enoxaparin injections difficult and INR monitoring with warfarin challenging after transitioning to home 6 weeks s/p acute sci.
ASIA is commonly used, however difficult to grade a muscle when it is spastic. Measures like FMA, Brunnstrome stages are available for cerebral lesions. They may not be appropriate here due to difference in pathology behind movement deficit.
I think that the vertebral column might damage the blade or making it completely impossible. Has anyone ever tried to do this?
When a patient with complete SCI (T6- ASIA A) complains of pain (burning) in lower limbs, how can it be managed? Should exercises be modified if a person with SCI complains of central pain?
Hi all, I am in need of a software platform that can do PCA on a dataset that consists of the following:
1103 data points
41 categories of data (three hierarchical levels, 6 categories at highest)
674 pearson correlation coefficients (r values)
8 - 24 df; range of degrees of freedom between comparisons, with categories having values for 16-41 subjects
I'm looking to have a simple PCA analysis with determination of approximately three components, with simple plot of cumulative/proportional variability of each component, and 2 or 3 axis plots of the datasets.
With this data available, what are my best options for statistical software and graphing?
My sincere thanks, Jared
In my experiments, I perform a complete spinal cord injury, in a mice model, then I label the CST in motor cortex with FluoroRuby. Two weeks after, I investigate at thoracic segments (Thoracic 10) of the spinal cord, the regeneration of CST fibers in the lesion site. At the lesion site, I found fluorescente signal localized in the regenerated CST fibers and in others cells at the lesion site, the question is if exists the possibility that the FluoroRuby located in the CST fibers could be acquired by others cells at the lesion site?
What is the nursing care of spinal cord injured patient in the scene of the accident, in the emergency-intensive care unit and in the long-term rehabilitation? I would like related references or books about spinal cord injury nursing/neurological nursing/neuroscience nursing...thank you in advance!
We are using fast blue as retrograde tracer (in spinal cord tissue of rats) which is blue in color. So, we need some nuclear stain which is not blue in color.
Women with spinal cord injuries (SCI) represent a rising population. Unfortunately, there is limited information about labor care and delivery for women with SCI.
In studies in the area of Adapted Physical Activity among other limitations is the low n. An example can be seen in a recent publication by Kinoshita et al. (2013). One hypothesis leading to interesting results seemed to reduce this problem. What else may be done?
Kinoshita et al. (2013). Increase in interleukin-6 Immediately after wheelchair basketball games in persons with spinal cord injury: preliminary. Spinal Cord. Spinal Cord, (12 February 2013) | doi: 10.1038/sc.2013.4