Questions related to Pain
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.
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?
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!!
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?
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)
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
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
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.
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.
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 email@example.com
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...
-Calculating the effect of a treatment-
I have the mean+- SD for both pre and post treatment
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?
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!
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.
- 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?
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?
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!
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.
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.
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
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!
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!
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)
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?
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?
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?
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) ?
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?
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 ?
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.
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.
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
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?
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.
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?
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
Retraction is a pain in publishing: Opening a debate on this ever-evolving and a topic of wide concern.
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)
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.
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.
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!
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!
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
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)
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?
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.
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?
In measuring pain across different categories of pain conditions, ie musculoskeletal and gastrointestinal, would one pain scale suffice or should different scales be used?
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.
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.
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
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?
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?
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?
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.
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'
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?
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?
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?
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?
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?
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?
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?
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.
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"?
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.)
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.
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.