Science topic

Pain - Science topic

An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.
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Born with club feet which were corrected by means of plastering within the 6 months of age. Current age 67 years. Suffering feet and ankle pain for over 3.5 decades. Habitual of a routine post dinner walk for about 3-4 km everyday. No pain killers used. Pain is normally bearable but sometimes gets severe and is normally relieved to bearable limits by warm water bath / contrast bath. Recent podiatric/orthotic investigation suggesting Charcot Feet.
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@Priyanka Sindwani
Thanks, ma'am. I'll be obliged if you could please advise the strengthening and stretching exercises.
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What mediation model should I chose
Hypothesis: Pain Catastrophizing Mediating the effect of Psychological Flexibility on Physical Functioning in Patients with Chronic Pain over time
I have one measure before starting acceptance commitment therapy (in an RCT), 6 months after, 12 months after, and now years after.
Could I use a longitudinal meditation model to look at the relationship between pain catstrophising, psychological flexibility and physical functioning over time?
Is latent difference score mediation appropriate?
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Thank you a lot for your in-depth answer. I will look into the sources you listed, as well as your article- congratulations on your publication. Yes, I have measures for all, at four different points in time.
S
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Hi! What is the difference between Complex Regional Pain Syndrome and regular pain? I am aware of the various symptoms. However, from a cellular standpoint, what is the difference? Any specific receptors/proteins involved? The muscarinic receptors? Thank you!!
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Chronic pain is also defined when the pain is severe or persistent after a tissue injury is restored. Complex regional pain syndrome (CRPS) is a chronic pain disorder in which severe pain occurs at a specific site after trauma.
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Assume that there are m number of patients. Each patient records his/her pain level in an ordinal scale (from "not at all" to "excruciating") at t_i time point fro i=1,2,...,n_i. Suppose that we want to know whether patients are improving with respect to time or not. Is there any existing literature to test that?
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Hi everyone,
we use this stimulation electrode together with a Digitimer for pain stimulation in an experiment. We got them from another lab, but the first one broke and we just have a limited amount, so I am looking for some more of them, but did not succeed so far. Does anyone know or has an idea where to get more of them?
Thanks a lot!
(The cables originally looked a little bit different. I stabilized them to last longer)
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Dear Andrew,
Your note caught my attention because your laser soldering device might offer a means to monitor the effects of narcotics on nociception. Can you send me copies of any of your research reports that illustrate how it works?
Many thanks,
Lewis Coleman, MD
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I performed an AChE inhibition assay using a spectrophotometer with a wavelength 412 nm. In my study, I'm using plant extract which is Ulam Raja as AChE inhibitor. And I want to know why absorbance for negative control is higher than absorbance for the test sample with plant extract?
What I understand about this reaction is in negative control, AChE will hydrolyse substrate Acetylthiocholine Iodide and formed thiocholine as product detected by DTNB. This means that high thiocholine formed will increase the concentration thus, the absorbance also increase. For sample absorbance that contain plant extract as AChE inhibitor, it will inhibit AChE from hydrolyse Acetylcholine Iodide and DTNB will detect less amount of thiocholine thus, the absorbance for sample test is lower than negative control. It's mean that higher concentration of plant will result in low thiocholine production and the absorbance becomes lower. Is it correct? sorry for my grammar error I hope you can understand what I try to explain
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The substrate you should be using for this assay method is acetylthiocholine, not acetylcholine.
If the negative control contains the same amount of plant extract, substrate, and DTNB in the same volume as the sample containing AChE, then there is no circumstance under which the negative control absorbance would be higher than the absorbance of the sample with AChE. This means that there has been a technical error in the sample preparation or measurement.
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I performed an AChE inhibition assay using a spectrophotometer with a wavelength 420 nm. In my study, I'm using plant extract which is Ulam Raja as AChE inhibitor. And I want to know why absorbance for negative control/ test sample is decrease or increase in spectrophotometer. What happen in the process
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Yoram Gerchman Alright, thanks again
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I’m curious if a newer theory on pain exists or whether we are still attempting to understand the theory fully in order to prove/disprove its correlation.
I understand it was a theory and required research to prove, however I’m not sure how a theory is proved if the medical establishment doesn’t still can’t successfully prevent or reverse the condition. Confirmation of a theory should balance recovery, reversal and management of pain through research studies, not simply pharmacological and pain management. We have severe chronic illnesses that fall distinctly in pain theory territory, for instance fibromyalgia a disease that has been coined “invisible“, abuses ones own body but can’t be tested or resolved and isn’t classified as an autoimmune condition. Yet the common information given to patients is we don’t understand fibromyalgia, nor how to reverse the condition. Some treatments are available to manage individual side effects of illness, generally consisting of seeing multiple disciplinary medical fields.
Central Sensitization Syndrome perhaps is a foundational stone in the theory. However I find it inconceivable with the advent of scientific medical research advancements (funded as part of the covid 19 pandemic), that this disease can continue to be discounted as a type of pandemic of various origins, given it often has certain known triggers ie infectious disease, PTSD And various other illness classifications.
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There is growing recognition that probably the vast majority of “benign” chronic pain presentations represent a brain problem rather than a problem with receptors.
Different researchers, depending on speciality, have investigated a variety of aspects, all of which point to 2 factors: conditioned triggers to actual pain signalling, and learned hypersensitivity in response to “normal” signals from receptors.
None of this research is related to the work or theories of Melzack and Wall.
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I have been treating this patient for 20 years. She is 80 years old now. In the past 10 years her degenerative scoliosis (DS) has progressively worsened. We did xrays before starting the combination of lumbosacral Flexion/Distraction (Cox Technic) and Fascial Plane Therapy. Her scoliotis improved almost 13.5 degrees. Her pain improved (NPS) 6-8/10 to 1-2/10. I cannot find anything in the literature, non-surgically, to compare this to.
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Thank you Francesca. The therapy I did on this patient is the same as an ultrasound video for a different patient with 34 years of chronic low back pain. It uses cine-loop to show changes in the connective tissue (thoracolumbar fascia) before and after treatment.
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Dear research community, we need your help. We are conducting a systematic and narrative review on conditioned pain https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021266688.. If you know of any report or paper (published or unpublished) on the topic, please contact  sahaj.kang@ugent.be
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Dear Yaakov,
Thank you so much for your reply and the suggestions. These studies seem to be about conditioned pain modulation (CPM) and hence different from what we are interested in, which is the associative learning procedure known as classical conditioning. We often find that these two are easily confused due to the almost identical names. Anyhow, your help is much appreciated.
Kind regards,
Sahaj
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I am auditing pain score outcomes in a pain clinic and need to hopefully show that the score on discharge is significantly better than on admission for most patients - I am not sure which test to use for this as my stats is pretty rusty. I always thought T-test was for two different groups with different interventions...
Thanks!
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You have to compare two dependent groups: admission vs. discharge. First, you should examine the distribution of variables with the Shapiro-Wilk test. If the distribution deviates from the normal distribution (p <0.05), use the non-parametric Wilcoxon test . For normal distribution (p> 0.05) use the student's t-test for dependent groups. Good luck
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Hi,
does anybody have information that can share about pain recognition in bats?
Citable sources will be especially appreciated.
Thank you
Javier
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Hi Carl
thank you for your suggestion. I am aware of these books, but I don't have access to them, unfortunately.
Javier
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-Calculating the effect of a treatment-
I have the mean+- SD for both pre and post treatment
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You can calculate it online. Check this link:
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A 35 years- old man without comorbidities presents an epigastrium severe pain that irradiates for back (3 years). He denies use of alcohol, hypertrigliciredemia, abuse of drugs, hypercalcemia, pancreatic cancer or cholelithiasis. She realized several exams as CT where was observed tail pancreatic mass with 4 X 3 cm of diameter without as wirsung dilatation as calcifications, this finding was also observed in MRI. As ERCP as Cholangio MRI are normals.He realized echo-endoscopy that confirmed this mass, but discarded any finding of neoplasm. Biopsy was realized, showing at histopathology an absence of tumoral findings from pancreatic neoplasms. Only severe inflamation with large fibrosis and destruction of canalicules was observed. Auto-imune pancreatitis by either imuno-histochemical analysis or serical levels of igg4 and NAF was discarded.
This patient still presents severe pain in daily use of opioids. The question is: Is there a place for pancreatic resection in this setting?
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Dear Colin. At first, thanks a lot for your comentaries. I fully agree with you. So, I think that there are these both indications which you wrote.
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I want to use the Visual Analog Scale for Anxiety (VAS-A) in my DNP project. I know the VAS for pain is public domain, however, I have been unable to find whether the VAS-A is also public domain. Does anyone know whether I need to get permission to use the VAS-A in my research and if so where I can get permission? Thanks!
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Hello, I have the same problem. Do you find something? Thanks, eva baudysova
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Hello, I would like to ask from everyone's perspective what is the biological relevance and impact if the neurons that are being affected by an exogenous stimulus is (1) peptidergic or non-peptidergic neuron, (2) and their respective class of nerve fibers?
Currently, I am still consolidating and distinguishing these concepts because I think these are important research questions in molecular and cellular neuroscience projects.
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If these are people, then a clinical response to the administration of naloxone is likely. If the experiment... is a microelectrode neuronal response also using blockade of opiate receptors.
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  • I intend to do a quasi-experimental research, which compared a control group with an experimental group in which I apply an intervention to perform pain relief, comparing in both groups, pain levels before and after venous puncture
What should my sample size be?
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N= 2 x K x {sd/(m1-m2)}^2
I think this will help you
mean difference the investigator wishes to detect = m1 - m2
standard deviation=sd
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In my last research, I investigate whether patients with musculoskeletal disorders had increased susceptibility to SARS-CoV2 infection or developed more severe forms of COVID-19; as well as whether COVID-19 affected the underlying disease.
Results showed that the frequency of COVID-19 was low and statistically nonsignificant, but that led to a worsening of the underlying disease.
What are your clinical impressions, ie do you have similar research results?
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COVID-19 and Its impact on the musculoskeletal system
Not only the people with musculoskeletal disorders are more susceptible to the COVID-19 pandemic (1), but musculoskeletal symptoms are one of the manifestations of COVID-19 illness (2). Furthermore, these disorders are also more common in people as long-term effects of COVID-19 (or long-COVID) (3-4).
Please have a look at these articles for evidence:
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Dear All,
I am writing a meta analysis. My data from the studies only shows Pre: Mean (SD) Post: Mean (SD) for both treatment and condition. I want to summarize their findings.
I can calculate the difference of means and the SE. However, because they use different scales for the outcome 1-10, 1-21 or 1-40 (for pain), I think I need to transfer it to SMD. But How do I calculate that? And consequently how do I calculate the SE for each SMD per study because I need to provide that in RevMan for the generic inverse variance...
Lots of thanks!
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I'm looking for co-authors Are you a master's or doctoral student in psychology, behavioural sciences, social work, counseling psychology or a related discipline and would like to co-author a study on the depth of emotional pain? If so, let's examine this together.
Have you ever wondered why people self-harm when they are in discomfort or emotional pain? Some curse injury by cutting or burning their flesh, punching or hitting oneself. They do this to divert attention away from the pain or to distract the brain. Can you fathom burning your skin in order to relieve emotional pain? We won't be able to grasp why individuals do what they do or how to help them unless we understand the depth of emotional agony. It is simple to discuss bodily pains caused by injury or illness. Non-physical pain, on the other hand, is difficult to discuss, and instant treatment is impossible.
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Before we start an article or research on emotional pain, I think we should look closely about the main components or dimensions that make up emotional pain, and through which we can find a treatment that enables us to overcome or alleviate it in the individual who suffers from it.
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I need to understand the fibromyalgia tender points and the relation between each other, according to the concept " If they fire together, they wire together". But all what I found by searching was only their positions and some information about pain/ diagnosis/relief,...
So I need a help with any reference even if just an opinion about this issue. Thanks a lot.
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Hi,
Some references:
Harth M, Nielson WR. The fibromyalgia tender points: use them or lose them? A brief review of the controversy. J Rheumatol. 2007 May;34(5):914-22. PMID: 1747747
Schneider MJ. Tender points/fibromyalgia vs. trigger points/myofascial pain syndrome: a need for clarity in terminology and differential diagnosis. J Manipulative Physiol Ther. 1995 Jul-Aug;18(6):398-406. PMID: 7595112
Turk DC, Flor H. Primary fibromyalgia is greater than tender points: toward a multiaxial taxonomy. J Rheumatol Suppl. 1989 Nov;19:80-6. PMID: 2691687
Honda Y, Sakamoto J, Hamaue Y, Kataoka H, Kondo Y, Sasabe R, Goto K, Fukushima T, Oga S, Sasaki R, Tanaka N, Nakano J, Okita M. Effects of Physical-Agent Pain Relief Modalities for Fibromyalgia Patients: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Pain Res Manag. 2018 Oct 1;2018:2930632. doi: 10.1155/2018/2930632
Staud R. Are tender point injections beneficial: the role of tonic nociception in fibromyalgia. Curr Pharm Des. 2006;12(1):23-7. PMID: 16454721
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16 year old female a known case of prematurity sequale with achilis tendon lengthening at age of 6
now presented with pain and numbness of left leg
by examination pyramidal sign all over
sensory impairement of ant thigh and leg
ncs show chronic tibial nerve injury
no history of trauma or infection
any suggestion?
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Tarsal tunnel syndrome
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Some patient refer ocular pain pre stroke case
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Good morning all! I am hoping to create a graph similar to Melzack's pain graph comparing the scores of two groups on one scale (Please see attached). I am trying to find out what is the name of this type of diagram, and how to create one. I use SPSS and can work with Excel as well. Thank you!
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I'm sure that you could do something in R or Python, but that looks like it was made manually. Inkscape would be a good option.
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My lab is looking for a reliable, valid measure of pain for our nonprofit-funded phase 1 clinical trial. We were originally considering the Brief Pain Inventory (BPI) but the paywall (~400) is a bit higher than anticipated. Has anyone had luck with other pain measures similar to the BPI but is either free or more budget-friendly? I did see the McGill Pain Questionnaire, but this appears to require a fee as well (still waiting to hear what that fee will be).
We are looking for a scale that reports both acute and more chronic pain, ideally including history of pain medication/treatment effectiveness. Hence, some of the scales that initially come to mind (e.g., visual analogue scale, numerical rating scale) don't seem like the best fit.
Any help would be appreciated, many thanks!
David
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Hello David,
Here are a couple of sources that might prove helpful for your search:
Good luck with your work.
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21-year-old female patient having shooting sciatic pain; stiffness in back; radiating pain through buttocks, hips, and legs; worsening pain with extended periods of sitting; some leg weakness. MRI demonstrates L5-S1 disc bulge with no nerve impingement. Diagnosed with degeneration of lumber intervertebral disc with degenerative disc disease and lumbar spondylosis. Surgery is not recommended, physical therapy not helping, cyclobenzaprine & other pain medication no longer working.
Backstory: "pulled" back in May of 2021 with excruciating, immobilizing pain. Got better in one week, pain is now constant.
(MRI & X-ray images included)
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What is the neurological status of the patient objectively (the "leg weakness")? With this MRI, a neurologic deficit should be further evaluated to rule out other causes of neurological involvement. Also, the SI joints should be evaluated as a possible pain generator (often causes b/l buttocks pain with radiation downwards, and with a pain pattern that worsens with prolonged sitting).
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Hi all, regarding WOMAC scores, I note most are presented as a aggregate score out of 96. Where 96 means more pain. As confirmed here:
However, why is it here - this shows the opposite where high scores means less pain/normal?
Which score is correct and how does one convert to the other?
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See perrin & Purcell 2009.
Not sure if this approach will suit your purposes. That should be 5 activities with 5 levels 0 - 4 (4 being most severe pain)
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I have measured pain intensity using numerical pain intensity scale (NRS) in intervals of 30 min upto 6h for 4 groups. The NRS scale is from 0-10. Can anyone guide me on what statistical comparison can I use to compare the 4 groups?
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One Way analysis of variance would be the right tool if the observations are atleast measured on an interval scale. If the pain intensity scores aren't ordered, then you may proceed with ANOVA or its non-parametric equivalent i.e. Kruskal Wallis Test(if the normality/homogeneity of variance assumption is violated). If the pain intensity scores are ordinal, then you must go ahead with Jonckheere Terpstera Test which is the analogue of ANOVA considering the ordinal nature.
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Dear All
I am interested in publishing a text summarising the research on pain in neuropathic patients with CRPS (medical literature). The article summarizes the experience of pain management and pain use as a diagnostic indicator. Are you planning a publishing in this subject?
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Ok. What will be Yours "center of gravity" fort this text?
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In many animal pain models, FCA (Freud's Complete Adjuvant) and carrageenan are injected (in the paw for instance) to induce an experimental immune response and then, assess inflammatory induced hyperalgesia. While carrageenan-induced hyperalgesia lasts a few days, FCA-induced hyperalgesia can last up to weeks using the same species and the same mode of administration.
What are the molecular mechanisms that drives such differences, knowing that CFA and carrageenan are different in nature (heat killed Mycobacterium tuberculosis and polysaccharide extracted from red seaweeds) ?
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Simon Bruce Perrin Again, most experiments on animals can be considered "torture", depending on your point of view. Does fear conditioning not cause pain, stress, and fear in animals?
Pain models like FCA have very little effect on the animals' well-being as measured by weight, grooming, socialization etc. In fact, usually you cannot distinguish between pain model animals and sham controls based on these well-being indices. You get much stronger effects on these indices when using other common paradigms such as repeated exposure to non-painful stressors (e.g., forced swim test).
We have ethics committees to deal with these issues, and fortunately we do not rely on one high-horsed person's opinion. Now please stop harassing research students in pain labs and clear the stage for people who might actually have helpful answers to their valid and interesting scientific questions. Good day
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Dear RG members,
There is doubt that teaching/ learning online has become a pain in the neck worldwide. The gap is getting bigger and bigger. How to bridge such a gap? How would one overcome the barriers of online learning/teaching?
Regards,
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Solution/resolution depends on the nature of problem faced by the individual in online teaching/learning.....
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Hi
what is suitable systems for scoring sciatica pain
Regards
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You could also consider the Sciatica Bothersomeness Index or Sciatica Frequency Index for a research context. I'm not sure how often these are used in clinical practice in comparison to the more common Oswestry / Roland-Morris type questionnaires which are more generic for low back pain:
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I have watched a child crying loudly in pain, while collecting blood for testing. Can we develop a technique which can collect the blood or inject a medicine to children in a complete pain-free way ?
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Thanks you, dear Dr.Mark Louis Weiss
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I'm a 4th year undergraduate in University Of Colombo School of Computing (UCSC) in Sri Lanka. I'm doing my final year research based on Taste and EEG data that is recorded of taste sensations. Where I was trying to find a public data set but couldn't find any. Does anyone know how can I find a EEG data set of Taste. Your responses and help will be much appreciated.
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You may be able to get data sets from articles:
Misra G, Wang WE, Archer DB, Roy A, Coombes SA. Automated classification of pain perception using high-density electroencephalography data. J Neurophysiol. 2017;117(2):786-795. doi:10.1152/jn.00650.2016
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I have a small but significant relationship between pain scores and risk of a certain condition (R^2=0.057, p=0.039).
When I include age and gender as covariates, the model loses all significance (R^2=0.043, p=0.15).
This suggests to me that age and/or gender explain at least as much of the variance in pain scores that risk does.
However, when the univariate regressions just of age and gender show no relationship at all (age R^2=0.017, p=0.8, gender R^2=0.005, p=0.4)
I cant quite wrap my head around what the potential relationships between the covariates might be.
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There might be a bit of collinearity indeed but that's normal if not all covariates/independent variables are perfectly balanced (I can imagine pain score to vary with age, and maybe gender).
  • One important question would be: does it matter? Given that the model without age and gender only explains 5.7% of the variance in the response, and the p-value is borderline, the result is already saying that pain scores don't say very much about the outcome... (Note: p-values also have uncertainty although it is not reported)
  • Collinearity has been almost "demonised" for a long time (I have been guilty too), but some have suggested recently that we should consider it part of reality (and increased uncertainty, reduced statistical significance) rather than trying to get rid of it...
Hope that helps making sense of collinearity and the result...
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My long term study of patients with fibromyalgia and diffuse type 2 occupational overuse syndrome during use of sEMG biofeedback shows that there is a symptomatic difference in pain
during splinting of muscles causing deep ischemic pain and the release of muscle tension which brings about numbness, pins and needles and deep throbbing pain. I am looking for an objective measurement to verify this
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The Treaty of Sleep Medicine, of the Spanish Sleep Society, published by the Editorial Médica Panamericana, is the first book written in Spanish on this discipline. In it, the subject of fibromyalgia and its relationship with sleep disorders is deepened with scientific evidence. The symptoms and discomfort caused by this disease are usually complex and difficult to approach, and they usually require the intervention of different professionals in the field of medicine and health: PATIENTS WITH FIBROMYALGIA ASSOCIATE PRIMARY SLEEP DISORDERS MORE OFTEN THAN GENERAL POPULATION.
Let's describe some key points to understand it a little more.
The characteristic symptoms of fibromyalgia are pain and fatigue. However, the majority of patients also have cognitive, mood and sleep disturbances, which is why these episodes have also been included in the diagnostic criteria for the disease.
The mechanisms involved in the development of fibromyalgia have an effect on sleep disturbances, but remain a source of research at the present time.
Fibromyalgia patients associate primary sleep disorders (insomnia, sleep apnea-hypopnea syndrome, periodic leg movements during sleep, and restless legs syndrome) more often than the general population.
Fibromyalgia patients frequently have mood or anxiety disorders, which in turn are accompanied by sleep disturbances. There seems to be a relationship between pain, mood disorders, and sleep disturbances.
There is no drug specifically approved for the treatment of sleep disturbances in fibromyalgia. However, duloxetine, pergabalin, and laamitriptyline are the most recommended by evidence-based guidelines. Sodium oxybate, a drug used for daytime sleepiness and cataplexy (sudden and usually brief episodes of bilateral loss of muscle tone during wakefulness), has performed very well in studies of fibromyalgia patients.
Melatonin is a molecule with the ability to regulate the sleep-wake rhythm and circadian rhythms or biological rhythms (oscillations of biological variables at regular intervals of time), so it could have beneficial effects in the treatment of fibromyalgia. This element has the ability to decrease the cadence of sleep and promote its continuity. Although at present there are favorable results due to its use –always under medical prescription-, the number of studies carried out is small.
Failure to achieve restorative sleep night after night, or systematically suffer from other sleep disturbances is related to a clinical worsening of fibromyalgia, so appropriate treatment can improve the overall symptoms of the disease.
If a dream is a wish, the fibromyalgia wish may be fulfilled by dreaming.!!!
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Hello!
In cases where I want to evaluate an overall measure, how could I combine two means from the same group?
Example: I have pain VAS for lower back and VAS for hips. I want to know the overall pain VAS. How could I proceed?
Thank you,
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I'm a 4th year undergraduate in University Of Colombo School of Computing (UCSC) in Sri Lanka. I'm doing my final year research based on Pain and EEG data that is recorded of pain. Where I was trying to find a public data set but couldn't find any. Does anyone know how can I find a EEG data set of Pain. Your responses and help will be much appreciated.
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Read the definition and description of pain from the IASP and you will see that it is ALWAYS somewhat SUBJECTIVE and PSYCHOLOGICAL ... in such a scenario, if the EEG IS NEVER A GOOD MEASURE OR A GOOD INDICATOR OF THE REALLY PERCEIVED PAIN, HOW WILL IT BE FROM SIMULATED OR FEELING PAIN?
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We are starting an investigation, in the field of physiotherapy, on the evaluation and clinic of pain.
We are interested in knowing which diagnostic evaluation scales are being evaluated.
We are also interested in knowing how to qualitatively assess pain: do you know interview protocols for patients with chronic pain?
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As we are now in 2021, the "ad hoc" relationship made by the "Pain" Magazine and, likewise, the one made by the IASP, whose website is: https://www.iasp-pain.org/
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We need your expertise/experience as a pain clinician, researcher or patient. We would like to hear your opinion about the learning of pain and others somatic sensations through this short survey https://limey.ugent.be/GHP272/index.php/263964?lang=en
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Dear Farooq,
Thank you for the suggestion. I am already in contact with EFIC and the next step is to get in touch with IASP. Good to know that it's been done before, will probably make it easier for me to get their help :) :).
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Retraction is a pain in publishing: Opening a debate on this ever-evolving and a topic of wide concern.
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In 2021, an article studying open source community by Qiushi Wu and Kangjie Lu at University of Minnesota was withdrawn after Linux Foundation found out that researchers submitted patches for Linux kernel with intentional bugs without obtaining appropriate consent
Wu, Qiushi; Lu, Kangjie (2021-04-26). "Retraction of paper" (PDF). Retrieved 2021-05-02.
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What's the verdict on regional analgesia in breast surgery?
Is there any need to use it at all?
The 2018 Cochrane review concluded that synthesis of 18 RCTs favoured regional anaesthesia for the prevention of persistent pain three to 12 months after breast cancer surgery with an OR of 0.43 (95% CI 0.28 to 0.68, 1297 participants, low‐quality evidence).
However, the recent 11-year RCT published in the Lancet 2019 with 2132 patients across 13 hospitals internationally showed there was no difference in incisional pain:
Incisional pain was reported by 442 (52%) of 856 patients assigned to regional anaesthesia-analgesia and 456 (52%) of 872 patients allocated to general anaesthesia at 6 months, and by 239 (28%) of 854 patients and 232 (27%) of 852 patients, respectively, at 12 months (overall interim-adjusted odds ratio 1·00, 95% CI 0·85-1·17; p=0·99). Neuropathic breast pain did not differ by anaesthetic technique and was reported by 87 (10%) of 859 patients assigned to regional anaesthesia-analgesia and 89 (10%) of 870 patients allocated to general anaesthesia at 6 months, and by 57 (7%) of 857 patients and 57 (7%) of 854 patients, respectively, at 12 months.
If it doesn't reduce chronic post surgical pain, is there any point in using it?
(Note: these studies involved paravertebral regional analgesia)
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In high risk patients para vertebral block in T2 and T4 level with or without serratus anterior plane block MRM can be done.. should be done under light sedation...
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Working in the sport and fitness industry since 20 years before studying in a post- graduate program on chronic non-cancer pain management (CNCP), questions raised up about potential therapeutic use of Androgen Anabolic Steroid (AAS).
If anybody knows if these sports enhancing performance agents (mostly known as sports doping agents) can help for CNCP relief ?
Since more than 20 years, mostly in the field of bodybuilding, I've been witness of devastating chronic pain syndrome such as Chronic Regional Pain Syndrome (CRPS), neuropathic pain and also MSK nociceptive somatic pain injuries happening on athletes. In a large proportion of injured subjects, those who continued to use supra-physiological dose of AAS seems to have a much better functionality than everyone else. I would add that the use of those doping agents allows the injured subjects with chronic pain to self-manage their pain condition a hundred times better than every other method, medication, muti-modal pain rehabilitation, regular HRT commonly used in chronic pain clinic and hospital. The users, or I would say, the abusers understand that a decade before now.
Looking what we have in the literature on that topic is fairly poor and limited. It seems to be a totally new spectrum of research in pain science, as on the ground AAS are often used for CNCP control.
Feel free to add your comments and impressions as in a brain storming reflexion. If anyone finds out publications on that topic please let me know. That research avenu is probably brand new, maybe cause of the toxicity and teratogen potentials of AAS ?
If anyone observed the same thing as I, just let me know.
JP
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Anabolic steroids are synthetic — that is, man-made — variations of the male sex hormone testosterone. The correct term for these compounds is anabolic androgenic steroids. Anabolic refers to muscle development, and androgenic to increase in male sexual characteristics. Some common colloquilas names of these are gear, juice, roids, and stackers AND THERE IS NO CLINICAL OR ECPERIMENTALLY CONTRASTED EVIDENCE THAT THEY ARE USEFUL IN ANY KIND OF PAIN.
Its use can lead to negative mental effects such as: paranoid jealousy (extreme and unreasonable jealousy), extreme irritability and aggression (“roid rage”), delirium (false beliefs or ideas), decreased good judgment and obsession.
But in addition to the mental effects, steroid use often causes severe acne. It also causes swelling in the body, especially in the hands and feet.
Long-term effects
The misuse of anabolic steroids can cause serious health problems - which can even become permanent - such as:kidney problems or kidney failure
tumors and liver damage enlarged heart, increased blood pressure, and altered cholesterol levels, all factors that can increase the risk of stroke and heart attack even in young people increased risk of blood clots.
... AND, ALTHOUGH EVERYTHING EXPOSED SHOULD BE DISSUASIVE "PER SE", THERE IS NO CLINICAL EVIDENCE, PROPERLY CONTROLLED AND ANALYZED, THAT ITS USE IS USEFUL FOR ANY TYPE OF PAIN ... EXCEPT WHAT MAY GENERATE THE CONSIDERED EFFECT PLACEBO!
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Is there any difference in efficacy and effectiveness of both vaccines of similar type.
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Yes painful pentavalent vaccine is more effective than Painless one....
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Does anybody have a dataset from a posture intervention that would allow for a correlation coefficient to be calculated between change in posture and change in pain? Particularly interested in forward-head posture and tension-type headaches.
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Here I attach a series of References on the subject:
  • Pope MH, Bevins T, Wilder DG, Frymoyer JW. The relationship between anthropometric, postural, muscular, and mobility characteristics of males ages 18-55. Spine (Phila Pa 1976). 1985 Sep;10(7):644-8. PubMed PMID: 4071274.
  • Franklin ME, Conner-Kerr T. An analysis of posture and back pain in the first  and third trimesters of pregnancy. J Orthop Sports Phys Ther. 1998 Sep;28(3):133-8. PubMed PMID: 9742469.
  • Nourbakhsh MR, Arab AM. Relationship between mechanical factors and incidence of low back pain. J Orthop Sports Phys Ther. 2002 Sep;32(9):447-60. PubMed PMID: 12322811.
  • O'Sullivan PB, Mitchell T, Bulich P, Waller R, Holte J. The relationship beween posture and back muscle endurance in industrial workers with flexion-related low back pain. Man Ther. 2006 Nov;11(4):264-71. Epub 2005 Jun 13. PubMed PMID: 15953751.
  • Christensen ST, Hartvigsen J. Spinal curves and health: a systematic critical  review of the epidemiological literature dealing with associations between sagittal spinal curves and health. J Manipulative Physiol Ther. 2008 Nov-Dec;31(9):690-714. doi: 10.1016/j.jmpt.2008.10.004. Review. PubMed PMID: 19028253.
  • Smith A, O'Sullivan P, Straker L. Classification of sagital thoraco-lumbo-pelvic alignment of the adolescent spine in standing and its relationship to low back pain. Spine (Phila Pa 1976). 2008 Sep 1;33(19):2101-7. doi: 10.1097/BRS.0b013e31817ec3b0. PubMed PMID: 18758367.
  • Meziat Filho N, Coutinho ES, Azevedo e Silva G. Association between home posture habits and low back pain in high school adolescents. Eur Spine J. 2015 Mar;24(3):425-33. doi: 10.1007/s00586-014-3571-9. Epub 2014 Sep 12. PubMed PMID:  25212451.
  • Chaléat-Valayer E, Mac-Thiong JM, Paquet J, Berthonnaud E, Siani F, Roussouly  P. Sagittal spino-pelvic alignment in chronic low back pain. Eur Spine J. 2011 Sep;20 Suppl 5:634-40. doi: 10.1007/s00586-011-1931-2. Epub 2011 Aug 26. PubMed PMID: 21870097; PubMed Central PMCID: PMC3175927.
  • Blog: https://www.bettermovement.org/blog/2014/does-bad-posture-cause-back-pain
  • Brinjikji W, Luetmer PH, Comstock B, Bresnahan BW, Chen LE, Deyo RA, Halabi S, Turner JA, Avins AL, James K, Wald JT, Kallmes DF, Jarvik JG. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2015 Apr;36(4):811-6. doi: 10.3174/ajnr.A4173. Epub 2014 Nov 27. Review. PubMed PMID: 25430861; PubMed Central PMCID: PMC4464797
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Piriformis syndrome (PS) is an elusive, benign medical condition. Patients usually complaint deep-seated gluteal pain with some aggravating and relieving factors. Regarding aggravating factors, prolonged sitting on the affected side, affected side lying, posture change - standing from sitting, forward bending, etc. are common, whereas walking relives pain somewhat, especially in chronic cases. In acute PS, patients have pain relieving posture finding difficulty, physicians also get confused it with more prevalent low back pain diagnosis, namely prolapsed lumbar intervertebral disc (PLID).
PS is a disorder of exclusion of clinical mimics and it has no definite cause; in literature, lumbar spinal stenosis, leg-length inequality, professional dancers, fibromyalgia, previous fall, blunt gluteal trauma, etc. are mentioned as its risk factors. Sporadic case reports and our recent systematic review addressed infective cause of piriformis muscle injury, where patients complain of clinical features unlike of PS. In piriformis muscle (PM) infection, patients report of persistent deep gluteal pain that doesn't change with posture, patients also have fever and raised laboratory inflammatory markers (raised WBC count, ESR & CRP). Moreover, there may be characteristic MRI changes in the deep-seated gluteal and pelvic structures including PM. Pain medications & PM stretching exercise don't help patient anyway, they need antimicrobials as well; when antibiotics don't work, surgical drainage of PM is required. Like in PS, intra-lesional steroid is contraindicated here. If piriformis pyomyositis is left undiagnosed and untreated precisely, life-threatening consequences may be the outcomes, hence we can consider the piriformis pyomyositis as the PM emergency.
What do you think?
Suggested reading :
1. Siddiq AB, Danny Clegg, Hasan SA, Rasker JJ. Extra-spinal sciatica and sciatica mimics – a scoping review. Korean J Pain 2020; 33:305-317.
2. Siddiq AB, Rasker JJ. Piriformis pyomyositis, a cause of piriformis syndrome – A systematic search and review. Clin Rheumatol 2019; 38:1811-1821.
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Apart from the infectious problems, already described and warned, the "pseudo-sciatica" due to lesions of the piriformis,
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Dear Community,
We are looking for an antibody that will bind to the outside of the tertiary structure of AChE. It must not bind to the inside of the tertiary structure of AChE.
So ideally, we need an antibody that meets the following criteria:
• reactivity for both rats and humans
• capable of working in an environment where proteins cannot be denatured
• capable of being used in vivo
• capable of binding to the outside of the 3D structure of AChE
In vivo use in this context does not imply that we intend to inject the antibody into an animal or human, but that we would like to bring it into contact with unfixed rat or human nerve tissue.
Assuming that we would get an antibody custom made: Is it possible to use the same antibody for both rat and human tissue?
Do you see any pitfalls in the experiment that we picture? We are mostly interested in the molecular feasibility.
Any help is highly appreciated!
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it is thought to be involved in the pathology of Alzheimer's disease (AD) by accelerating the assembly of Abeta peptides into fibrillar species through forming complexes with Abeta via the peripheral anionic site on ACHE.
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I'm looking into a possible correlation of some types of chronic pain (those related to ptsd and mood disorders) correlating with balance issues, one-sided pain, or inner ear damage. Thanks for any help!
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Have you looked at studies including the VA population? Im not familiar with any specifically noting vestibular problems but I know the chronic pain and mental health overlap has been documented in this population. Good luck!
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Hello, Everyone. Greetings of the day valuable members of the group. Hope you all are doing well.
I would start this conversation with this statement that, a researcher only knows the pain of another researcher and I believe we all are researchers because we all do research at some point in time. I hereby would like to seek your valuable response to a set of questions in connection to my Research. Kindly spare 5-10 minutes and share your opinions. If you can circulate among your friends, I would be glad to have their responses as well. Thanks a lot in advance. https://docs.google.com/forms/d/e/1FAIpQLSebnXJcW-18LcLkgyg65o11I-0yatIT3Ey3yMS4BGNE9KbTEA/viewform #research #sustainability
#circulareconomy #consumerbehavior #greeneconomy
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I have already responded!
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Many clinicians have noted nonspecidfic pain modulating effects of injecting NACL0.9% or sterile water or another sterile solution which is considered inactive (used in the control group).
It is hypothesized that subcutaneous and intracutaneous injections modulate pain through:
1/ Dry needling effect: the effect of the needle which penetrates the skin and or muscle tissue such a 1A/ s the bleeding effect (blood contains platelets and growth factors), 1B/ triggerpoint effect when needling myofascial trigger points, 1C/ Gate control effect, 1D Effect on neuroinflammation, TRPV1 receptors,
2/ Volume effect: expansion of the extracellular space stimulates peripheral nerve endings
3/ Placebo effect (the placebo effect of an injection is bigger than a pil, but the effect seems to lessen after repeated sessions)
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In a clinical setting it is probably mostly explained by #3, the placebo effect. A patient has an expectation that they will feel better when they take a pill or are injected with something, because for your entire life before the sham treatment that has been the case. So, you get your sham treatment and feel better the first time because you have the mindset that you will. But, you figure out after a few times that nothing is actually happening, which explains the tapering effect over multiple treatments (extinction).
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Pain is such sign/symptom that any patient can describe it as high or low although he/she have no pain.
I know there are many pain provocation MSK tests but patient can also express it as false.
Is there any tool to assess pain severity, which patient exactly have, not that patient describe?
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No, not at all, according to the IAPS itself pain IS ALWAYS A SUBJECTIVE SENSATION AND PERCEPTION (in fact, as it says in its famous definition / conceptualization of pain).
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My mother, aged 39, has chronic genetic pancreatitis since at least 15 years. She has known several episodes of severe pain and went through lots of surgery that were unsuccessfull. She had a total pancreactomy in may 2020 followed by months of non-pain. But it came back. Because of the surgery, she has, of course, diabetes. She has also gastroparesis but the doctors seem to think that it is not the origin of pain, althouth they are not sure. Her stomach swells before the arrival of pain, like a 6 months pregnant woman. She evaluates her pain at 10 at day and at 12 on the evening on a scale of 10. To relieve pain, she has lots of medicine like Tramadol and other morphine derivatives. The doctors are searching for the cause of the pain but they cannot find. Her life quality is diminished et she suffers a lot. If you have any leads or articles that could help my mother, I would be grateful.
If you can help me or share this post, it would be amazing. Thanks.
Delannoy Manon
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The causes may delayed gastric emptying The stomach will take much longer than usual to empty its contents because of the surgery. This condition often resolves itself in seven to 10 days as the stomach begins to heal and resume its normal functions. If it does not, your surgeon will discuss the best way to treat this situation.
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Can anyone guide me on the pain areas in cloud computing where Operations Research techniques can be applied. Please guide me on this.
Regards,
JP
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A more recent survey (but also already quite some years old) is the following:
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Several organizations do not recommend aspiration when administering vaccines because no data exist to justify the need for this practice. They argue that: 1) Aspiration is more painful for the patient, 2) IM injections are not given in areas where large vessels are present, so the inadvertent intravascular injection is improbable and 3) There is no reports of a vaccine being administered intravenously and causing harm in the absence of aspiration.
However, 1) there seems not to be more pain in the adult in relation with aspiration (Taddio et al. Procedural and Physical interventions for vaccines injections: systematic review of randomized controlled trials and quasi-randomized controlled trials. Clin J pain, 2015), 2) the inadvertent intravascular injection is relatively frequent with 40% of the nurses claiming blood aspiration, and this is not exclusive of dorso gluteal site –dorso gluteal (15%) vs deltoid (12%)— (Cristine M Thomas. Blood Aspiration During IM Injection. Clinical Nursing Research 2015) and 3) such reports justifying security do not involve many patients, not consider secondary effects in the long run and not consider a potential decrease in efficacy of the vaccines -- intravenous administration seems to produce a rapid antigen depletion-- (Sissons H. Aspirating during the intramuscular injection procedure: a systematic literature review. Journal of Clinical Nursing 2015).
Are we doing it right?
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Yes right
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In measuring pain across different categories of pain conditions, ie musculoskeletal and gastrointestinal, would one pain scale suffice or should different scales be used?
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Normally yes: According to the IAPS itself, pain and its perception are ALWAYS subjective; Therefore, the Visual Analogue Assessment Scales (AAV) are adequate and sufficient for the assessment of any type of pain; For this reason, they are the most used in Pain Units and Clinics around the world.
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Hi. Just a quick question for the good statistics friends out there.
I am building a study in which I will measure a variable (say, anxiety) and then see how pain after surgery behaves in time. My hypothesis would be that patients with a greater level of anxiety before surgery will experience greater pain in time after it.
I know I could just make a distinction between a number of groups (e.g. no anxiety, mild anxiety, and so on) and then conduct a Repeated Measures ANOVA. But I wanted to know if there is a possibility to correlate the variable in an interval-level fashion instead of downgrading it to an ordinal-level variable. Think kind of a "Spearman correlation but for a time series", so to speak. How can that be done?
Also, is there a way to control for a variable with that design? For example, can I control for the variable gender, as has been suggested that males tend to have a higher anxiety profile before surgery?
Thanks a lot.
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I would look into GEE (Generalized Estimated Equations). I have had some luck using that model to look at increased output over time.
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Is this saying true that psychological trauma causes pathological diseases? As we all know mental health is as important as physical health. People use to believe that diseases appear after some sort of psychological pain.
All the comments and point of views are welcome.
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  • Thank you for this interested discussion Dr Ghulam Yaseen
  • I assume that's true because PTSD is A systematic disorder. In other words (Brain and body are closely linked in disease as in Health), such concept had been creating an overlaid area between medicine and Psychiatry. PTSD can alter psychophysiological reactivity, then impacted the performance of the somatic domain that may cause certain systematic abnormalities e.g gastrointestinal disorders and abnormal respiratory function.
  • Agreed with Humam Hamada Muslih
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A 30-year-old woman is seen by her physician. She has a temperature of 101°F and reports nausea and headache, with flank (below ribs and above iliac crest) tenderness and pain. When asked, she states that urination is sometimes painful, that she must urinate much more frequently than usual, and that she has a sensation of urgency. A random, midstream clean catch urine specimen is collected for a routine urinalysis and culture. The condition is
acute pyelonephritis
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Personnally I do not think so.
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Dear community,
I would like to conduct an experiment on the use of VR to reduce (the attention paid to) pain. While there are many studies on this topic, it is very hard to know what software/game is the most appropriate. It is clear that the most involved and immersed in VR, the less the user has a chance to pay attention to the pain. But too immersed experience might not fit some medical settings (if the patient is not supposed to move too much).
To summarize, can anyone recommend some games or software for research purposes?
Many thanks
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Any time be interested in how your research progresses
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Clinically it has been observed that some patients present with severe knee pain on one side and mild or no pain in other knee, on xrays Grade IV is not that painful as Grade III. So what are the possible reasons?
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Inappropriate postural/kinesthetic awareness leading to overloading plus poor conditioning of muscles on painful side.
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I have been working on a pain intensity study and I wanted my patients to report their pain intensity using numerical rating scale. many patients have reported thier pain in spectrum like 2 to 3 or 3 to 4. How should I interpret those data? Considering the data as 2.5 and 3.5 respectively for example?
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I agree with Jeremiah. I would like to mention that it is possible to distinguish between patients who tend to rate their pain highly and those who don't, ie the stoics. Years ago my colleague Shaun Kilminster invented a scale for patients to record their levels of anger, fatigue and depression (AFD) because they are increased in chronic pain such as arthritis of the knees, and he found a dichotomy when some record high pain scores but had no change in AFD (non-stoics) while others had marked AFD disturbance but still rated their pain low (stoics). The point is that the the anti-stoics produce big placebo responses so, if they are too numerous in your control group of a clinical trial, they make your analgesic look ineffectual.
See this paper on the Short Pain Inventory and the effect of topical NSAIDs on knee pain: Kilminster SG, Mould GP. Comparison of diclofenac spray and gel on knee joints of patients with osteoarthritic pain. Clin Drug Invest. 1999;5:345–54.
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The Paolo Procacci Foundation, a foundation whose aim is to increase research and developments in Pain Medicine, is trying to develop new knowledges on inflammatory pain.
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I am interested in being part of the Advisory Board, my email: mpcalimag@ust.edu.ph
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I am injecting different serotonergic drugs into mice i.p. and see an effect in the brain electrophysiology quite fast, i.e. within minutes, when using a specific receptor agonist drug. I do not see any effects of the other serotonergic drugs I've tried, nor of saline injections on the activity of the region I'm measuring, which to me indicates that the effect is not due to the injection itself (some pain response etc.), but rather that the specific agonist reaches the brain within 2-5 minutes and exerts an effect on the activity quite quickly. I know how fast the drug reaches the brain will highly depend on the nature of the drug, and probably many other factors, but was wondering if there is some general minimum time it takes for an i.p. injected drug to reach the brain.
All I've found is the paper below, in which after 5 minutes, changes are seen in dialysates:
'Ethanol and Acetaldehyde After Intraperitoneal Administration to Aldh2-Knockout Mice-Reflection in Blood and Brain Levels'
Thanks!
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Dear Claire, in pharmacokinetic and pharmacodynamic studies, the body usually is separated into different compartments that have different transfer functions for the passage of a drug (different animal models are described elsewhere in the literature). There are several reasons for a disappearance of drugs from the peritoneal cavity upon injection and for the delay a drug reaches the target area. Reasons can be for example diffusion into the surrounding tissues, the compound may be carried away by capillary blood or lymph, metabolized by tissue enzymes or bound to tissue proteins. So basically, one needs to consider a schematic block diagram of the absorption pathways for small and macromolecules from the peritoneal cavity to systemic circulation up to the brain (e.g. i.p. injection, peritoneal cavity, interstitium, capillaries, blood-brain barrier, etc.). You are right when you state that “…how fast the drug reaches the brain will highly depend on the nature of the drug, and probably many other factors…”. The drug has to pass different barriers and each barrier has a different time constant. Shoyaib et al. have published a paper concerning this matter in 2019 (Abdullah Al Shoyaib , Sabrina Rahman Archie , Vardan T Karamyan; Intraperitoneal Route of Drug Administration: Should it Be Used in Experimental Animal Studies?; Pharm Res (2020) 37: 12; https://doi.org/10.1007/s11095-019-2745-x). In this paper the authors discussed, if intraperitoneal route of drug administration should be used in experimental animal studies. The authors summarize the main mechanisms involved in bioavailability of i.p. administered drugs and provide examples of pharmacokinetic profiles for small and large molecules in comparison to other routes of administration. For example, the authors describe, that following rapid absorption from the peritoneal cavity, a compound may face one of the following two pathways to reach systemic circulation: 1) it is absorbed through the visceral peritoneum, the mesentery and omentum and is drained into portal circulation, or 2) the compound gets into the systemic circulation directly bypassing liver when it is absorbed through parietal peritoneum and lymphatics. As you can see there are many factors influencing the passage of an i.p. administered drug through all body compartments and therefore I think it is difficult to determine a reproducible general minimum time it takes for an i.p. injected drug to reach the brain. I hope that this paper will help you to answer your question. Good luck, Dirk
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I'm looking for a dataset of eeg recorded during the pain stimulation (prefered the cold pressure pain stimulation). Anyone can help me to find it?
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please see the link below it may be helpful
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Hello everyone,
Is it scientific to categorize continuous score obtained after using the standard tool if the tool developer had not categorized it? For example, Visual Analogue Score (VAS) is a continuous score obtained after patient assessment and it ranges from "0-10". 0 is considered as no pain and 10 is considered as high pain but in the literature, we can find that the obtained final VAS is categorized into Mild, Moderate, and Severe pain on the basis of quartiles range (Q1, Q2, and Q3).
If it's not scientific what are the different possible ways to analyze these kinds of data further in the different models?
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Thanks to you, dear Dhirendra Nath
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I have collected time series data for four single case experiments to evaluate the effects of an intervention of chronic low back pain. One of the participants pain levels appears to demonstrate micro-seasonality in the plotted data by fluctuations every three weeks.
My rudimentary understanding is: data seasonality and micro seasons is a term used to describe rhythmical' fluctuation's in time series data in sales and economic analyses.
An experience of micro-seasonality in pain level is logical for people with persistent non-specific pain as their activities and stress levels fluctuate with habits and physiological states. Has this been observed in any pain research?
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YES, OF COURSE !, especially in situations of intense cold, humidity or both together (among others).
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My mom (55 y.o.) has been sick with covid-19 for 10 days.
She had very mild fever(37.2degC) for the first 2 days. She took Nimesil just in case it keeps increasing. Then for the next 7 days she didn’t have any fever and she didn’t took any medicine, but she was having extreme fatigue. She has been feeling very unwell and we can’t figure out what exactly is wrong: she doesn’t have any pain, she has no difficulty breathing, her saturation is around 97%, she had no cough or anything, she didn’t loose her sense of smell/taste. But very often she would have her body temperature going down to 35.8-36.0.
And now, after 9-10 days, all of a sudden, she has fever with 38degC and she still has extreme fatigue, can someone explain what’s going on? Is it normal?
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I think its normal for covid19 patients, I saw patients have fever up to 14 days with no other symptom only fatigue, u should check her CBC, LDH, CRP, Ferritin, and D Dimer just to make sure everything is fine
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I will often use diagnostic blocks of various structures to diagnose pain syndromes.  Most medications I inject will last between 4-6 hours.  There are others that do not reach the peak of action until around 8 hours.  I wonder if there is a pain perception difference if I were to injection a faster acting/shorter duration anesthetic versus a slower acting/longer duration agent.
I've looked around but have not run across this research specifically.
Does anyone have insight or research to point me towards?
Thank you!
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Yes: Of course. In fact, one of the main classifications of pain is based precisely ON ITS DURATION TIME, being -according to the IAPS- considered as "ACUTE" that which lasts less than six months, this does not present special clinical or treatment problems and, as CHRONIC one that lasts more than six months and, unfortunately, does not respond well to painkillers, is usually associated -as a consequence- with depression, pain behaviors, hopelessness, a decrease in the capacity of the immune system, sleep disorder and a long etc., for all this it is a serious problem for Algiology and must be considered in itself and regardless of its etiology as a Disorder and a Health Problem in itself
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I am contributing to local guidelines and my local population has a high Pakistani diaspora (1st and 2nd generations). My experience suggests that they present with more cognitive and mood symptoms than pain. Pain being a secondary concern. Does anyone have any similar experiences or advice?
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Thank you, dear Asim Suleman and equally
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Hello!
I am currently conducting some correlational reserarch regarding stress, pain and work ability. I have measured stress with KEDS and PSS, pain with ÖMPSQ and work ability with WAI. I want to perform a multiple regression analysis with work ability (WAI) as the outcome variable and stress (KEDS and PSS) and pain (ÖMPSQ) as the predictor variables.
My question regards what i should do with the 2 different scales measuring stress (KEDS and PSS), do i run them as 2 separate predictor variables or do i add them together somehow as one variable, and if so, how do i do that easily in SPSS?
Best regards,
Johannes
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Multiple regression is the good option. You can enter both predictors simultaneously (enter method) or enter both predictors one by one if you have a literature support (hierarchal method). You can see the details in the book (Discovering Statistics Using SPSS by Andy Field), chapter 7
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I am looking for studies that show an association between PTSD recovery and whether it translates into improvement in the following areas:
- Improved cognitive function
- Improved pain interference
- Improved symptoms of depression
- Improved neuropsychiatric symptoms
If anyone is aware of studies in this area, please send my way.
Thanks!
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This book might also be helpful: Neuropsychology of PTSD: Biological, Cognitive, and Clinical Perspectives edited by Jennifer J. Vasterling, Chris Brewin
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In order to fulfill criteria for Somatic symtom disorder (DSM 5) a patient needs to be preoccupied with symtoms or their health. Reasonably a symtom like pain does make you preoccupied to some degree. So how have researchers tried to operationalize "preoccupation"?
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As a logical, normal and adaptive worry or affliction and not as an irrational, hysteroid or hypochondriac cognitive-emotional nanifestation ... moreover, I would classify it as a healthy response and, I reiterate, ADAPTIVE
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Hi everyone,
I'm trying to figure out the best way to set up my database in R for mixed model logistic regression analysis. This study is a longitudinal cohort study with repeated measures: each patient has had 1 or more surgical interventions, for which we want to analyze risk factors associated with post-operative pain.
Dependent (binary) variable: post-operative pain (yes/no)
Independent variables (examples):
- continuous e.g. age
- categorical e.g. sex (female/male), pain medication administered (none, paracetamol, NSAID etc.)
My questions:
1. Is it necessary to dummy-code independent variables to make it into dichotomous variables?
2. How would I go about entering random/fixed effects into this model? Any pointers on which variables to choose for random/fixed effects?
Your help and feedback would be very much appreciated.
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1. No. You can do that or you can create a factor (or ordered factor) from that variable. That allows you to change contrast coding using options and may help with labelling output. e.g., for a basic example: df$group_factor <- factor(df$group)
2. It depends what package you are using. For example for lme4 syntax:
glmer(y ~ 1 + group_factor + (1|clinic), family='binomial', data = df)
Random effects depend on the sampling context. So for the above example clustering of patients in clinics is assumed. You might also have repeated measures within person and patient would be a random effect (probably nested in clinics). In terms of random slopes it depends on what you are trying to do, though it can be difficult to estimate models with multiple random effects and complex covariance structures arising from random slopes and the covariance between slope and intercept.
e.g., glmer(y ~ 1 + group_factor + (1 + group_factor|clinic), family='binomial', data = df)
At a certain point it might be sensible to look at MCMC estimation if you are dealing with complex random effect structures.
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I've just unclicked the export map options (advanced options?) and can't get them back. I'd assumed you'd be given the choice of displaying them again, but they are nowhere to be seen. I now can't choose what file type or resolution to use, which is a huge pain.
Humble requests to resolve this problem. Thanks in advance.
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Hello Md Hafijur Rahaman Khan. A time ago i faced the same problem. In my case i was dealing with a bug. By deactivating the "advanced options" the size of this window was set to zero and there was no option to display it again. In my case a very easy workaround helped.
"Open the Export Map window and put the cursor in the File Name section.  Hit the Tab key 4 times to activate the options button that is hidden. This button should be right after the "Cancel" button. Press space bar once to expand the option section.
(Via the Tab key you jump from one button to the next)
I hope this solution also works in your case.
Best regards Paul