Pain Ladder By Who

30.06.2023 Chukwudi Eze 0 Comments

Contents

- 0.0.1 Who is the original pain ladder?
0.1 What is the WHO 3 step analgesic ladder?
0.2 Is the WHO pain ladder still valid?
- 0.2.1 What is the who ladder?

1 Who invented the pain?
2 What is the reverse pain ladder?
- - 2.0.1 What is the safest pain medication to take?
- 2.1 Who created the 1 10 pain scale?
3 Who defined pain?
- - 3.0.1 Who is the father of pain killer?
4 What is the original pain theory?
- 4.1 What is the original pain theory?
5 What is pain real name before death?
- 5.1 What is the reverse pain ladder?
- 5.2 Who is pain master?

Who is the original pain ladder?

By the ladder: If pain occurs there should be prompt administration of drugs in the following order: non-opiods (e.g. acetaminophen) as necessary, mild opiods (e.g. codeine) then strong opiods (e.g. morphine or hydromorphone) until the patient is free of pain.

What is the WHO 3 step analgesic ladder?

WHO Analgesic Ladder and Opioid Crisis – The World Health Organization (WHO) first released a document addressing cancer pain relief in 1986, which stipulated a Three-step analgesic ladder as the guideline for developing treatment plans for cancer pain.22 It was revised in 1996.23 Prior to the guideline’s release, many patients suffered from unnecessary pain due to the stigma and fear associated with both the prescription of opioids and their utilization.24 The WHO analgesic ladder specifies treatment on pain intensity, from simple analgesics for mild pain to opioid analgesics for moderate and severe pain. Its three steps are: Step 1 Non-opioid plus optional adjuvant analgesics for mild pain; Step 2 Weak opioid plus non-opioid and adjuvant analgesics for mild to moderate pain; Step 3 Strong opioid plus non-opioid and adjuvant analgesics for moderate to severe pain. It is advised to move up one step when there is persistent pain. In case of toxicity or severe adverse effects, providers are advised to either reduce medication doses or move down one step. The ladder provides five simple recommendations for the usage of analgesics: by mouth, by clock, by ladder, by individual and attention to the detail. Just two years following its release, it was already validated in 80–90% of cases.25 The stepwise approach had tremendous value when it was introduced for its conservative and simple principles for pain management, which could be applied everywhere in the world, even in those underdeveloped countries with fewer pain management specialists. It has been of significant benefit for the control of pain worldwide. Until now, this guideline has remained applicable, not only in cancer pain management but also for acute pain and chronic pain requiring analgesics.26 The three-step ladder for cancer pain has also been commonly employed in CNCP, which very likely contributed to opioid analgesic overuse and escalation.26, 27 For ensuring patients with safer and more effective chronic pain management, the CDC in 2016 released a guideline regarding the prescribing of opioid pain medication for adult patients with CNCP in the primary care setting. The concept of pain relief as a fundamental human right acknowledges access of patients to essential medicines, including opioid medications for the management of pain. According to the WHO analgesic ladder, the provider prescribes opioid analgesics to patients based on the patient’s report of how serious the pain is. In the United States, the top 4 opioids prescribers are physicians in family practice, internal medicine, and nurse practitioners, and physician’s assistants, with the majority of them not specifically trained in pain control to a significant degree.14, 28 – 30 It has been shown that chronic pain patients obtain opioid medication easily from physicians.2, 31 A study in 2014 reported that patients received opioid analgesic prescriptions from two providers in 34.6% of cases, 14.2% from three providers, and 11.9% from four or more prescribers.32 There were 240 million opioid prescriptions dispensed in 2015 in the United States, almost one for every adult in the general population.33 Prescriptions thus have probably been a major contribution to the issues of opioid addiction and overdose deaths.34 Furthermore, some physicians prescribe more than one-month of opioid medication to patients, 35 while too many patients leave hospitals with bottles of unnecessary opioid analgesics.2 There are many cases of nonmedical users of opioids obtaining them from their relatives or friends, just for experimentation or for “getting high”.36 United States poison control centers reported 188,468 prescription opioid exposures among children aged <20 years old from 2000 to 2015.37 More than 2,000,000 people are suffering from prescription opioid-related substance abuse currently, 38 which highlights the fact that this is a particularly devastating problem in public health. Therefore, how to prescribe the opioid analgesics appropriately can be particularly challenging and stressful for primary care providers. Changes in opioid prescription policies should include sufficient training, including the applicability of analgesic ladder, which is a valuable guideline addressing both cancer and non-cancer pain.

Is the WHO pain ladder still valid?

References – 1. Ventafridda V, Saita L, Ripamonti C, De Conno F. WHO guidelines for the use of analgesics in cancer pain. Int J Tissue React.1985; 7 (1):93-6.2. Jadad AR, Browman GP. The WHO analgesic ladder for cancer pain management. Stepping up the quality of its evaluation.

JAMA.1995 Dec 20; 274 (23):1870-3.3. Orhan ME, Bilgin F, Ergin A, Dere K, Güzeldemir ME. Agri.2008 Oct; 20 (4):37-43.4. Araujo AM, Gómez M, Pascual J, Castañeda M, Pezonaga L, Borque JL. An Sist Sanit Navar.2004; 27 Suppl 3 :63-75.5. Dworkin RH, O’Connor AB, Backonja M, Farrar JT, Finnerup NB, Jensen TS, Kalso EA, Loeser JD, Miaskowski C, Nurmikko TJ, Portenoy RK, Rice ASC, Stacey BR, Treede RD, Turk DC, Wallace MS.

Pharmacologic management of neuropathic pain: evidence-based recommendations. Pain.2007 Dec 05; 132 (3):237-251.6. Moulin DE, Clark AJ, Gilron I, Ware MA, Watson CP, Sessle BJ, Coderre T, Morley-Forster PK, Stinson J, Boulanger A, Peng P, Finley GA, Taenzer P, Squire P, Dion D, Cholkan A, Gilani A, Gordon A, Henry J, Jovey R, Lynch M, Mailis-Gagnon A, Panju A, Rollman GB, Velly A., Canadian Pain Society.

Pharmacological management of chronic neuropathic pain – consensus statement and guidelines from the Canadian Pain Society. Pain Res Manag.2007 Spring; 12 (1):13-21.7. Tramèr MR, Carroll D, Campbell FA, Reynolds DJ, Moore RA, McQuay HJ. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review.

BMJ.2001 Jul 07; 323 (7303):16-21.8. Attal N, Cruccu G, Baron R, Haanpää M, Hansson P, Jensen TS, Nurmikko T. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision. Eur J Neurol.2010 Sep; 17 (9):1113-e88.9. Vadalouca A, Moka E, Argyra E, Sikioti P, Siafaka I.

Opioid rotation in patients with cancer: a review of the current literature. J Opioid Manag.2008 Jul-Aug; 4 (4):213-50.10. Di Napoli R, Esposito G, Cascella M. StatPearls, StatPearls Publishing; Treasure Island (FL): Jul 26, 2022. Intrathecal Catheter.11. Cascella M, Muzio MR, Viscardi D, Cuomo A. Features and Role of Minimally Invasive Palliative Procedures for Pain Management in Malignant Pelvic Diseases: A Review.

Am J Hosp Palliat Care.2017 Jul; 34 (6):524-531.12. Kanpolat Y. Percutaneous destructive pain procedures on the upper spinal cord and brain stem in cancer pain: CT-guided techniques, indications and results. Adv Tech Stand Neurosurg.2007; 32 :147-73.13.

Cahana A, Mavrocordatos P, Geurts JW, Groen GJ. Do minimally invasive procedures have a place in the treatment of chronic low back pain? Expert Rev Neurother.2004 May; 4 (3):479-90.14. Samuelly-Leichtag G, Adler T, Eisenberg E. Something Must Be Wrong with the Implementation of Cancer-pain Treatment Guidelines.

A Lesson from Referrals to a Pain Clinic. Rambam Maimonides Med J.2019 Jul 18; 10 (3) 15. Stjernswärd J. WHO cancer pain relief programme. Cancer Surv.1988; 7 (1):195-208.16. Szeto CC, Sugano K, Wang JG, Fujimoto K, Whittle S, Modi GK, Chen CH, Park JB, Tam LS, Vareesangthip K, Tsoi KKF, Chan FKL.

Non-steroidal anti-inflammatory drug (NSAID) therapy in patients with hypertension, cardiovascular, renal or gastrointestinal comorbidities: joint APAGE/APLAR/APSDE/APSH/APSN/PoA recommendations.
Gut.2020 Apr; 69 (4):617-629.17.
Cascella M, Quarto G, Grimaldi G, Izzo A, Muscariello R, Castaldo L, Di Caprio B, Bimonte S, Del Prete P, Cuomo A, Perdonà S.

Neuropathic painful complications due to endopelvic nerve lesions after robot-assisted laparoscopic prostatectomy: Three case reports. Medicine (Baltimore).2019 Nov; 98 (46):e18011.18. Lippe PM, Brock C, David J, Crossno R, Gitlow S. The First National Pain Medicine Summit-final summary report.

Pain Med.2010 Oct; 11 (10):1447-68.19. Leung L. From ladder to platform: a new concept for pain management. J Prim Health Care.2012 Sep 01; 4 (3):254-8.20. Cuomo A, Bimonte S, Forte CA, Botti G, Cascella M. Multimodal approaches and tailored therapies for pain management: the trolley analgesic model. J Pain Res.2019; 12 :711-714.21.

Melzack R. Pain and the neuromatrix in the brain. J Dent Educ.2001 Dec; 65 (12):1378-82.22. Crush J, Levy N, Knaggs RD, Lobo DN. Misappropriation of the 1986 WHO analgesic ladder: the pitfalls of labelling opioids as weak or strong. Br J Anaesth.2022 Aug; 129 (2):137-142.23.

Guiloff RJ, Angus-Leppan H. WHO analgesic ladder and chronic pain: the need to search for treatable causes. BMJ.2016 Feb 04; 352 :i597. Disclosure: Aabha Anekar declares no relevant financial relationships with ineligible companies. Disclosure: Joseph Maxwell Hendrix declares no relevant financial relationships with ineligible companies.

Disclosure: Marco Cascella declares no relevant financial relationships with ineligible companies.

What is the who ladder?

The WHO pain ladder (Figure 1) describes pain in terms of intensity and recommends that analgesics be prescribed starting at Step 1 (nonopioid analgesics, such as acetaminophen or non-steroidal anti-inflammatory drugs ).

Who invented the pain?

Historical – Before the relatively recent discovery of neurons and their role in pain, various different body functions were proposed to account for pain. There were several competing early theories of pain among the ancient Greeks: Hippocrates believed that it was due to an imbalance in vital fluids, In 1644, René Descartes theorized that pain was a disturbance that passed along nerve fibers until the disturbance reached the brain. Descartes’s work, along with Avicenna’s, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as “a specific sensation, with its own sensory apparatus independent of touch and other senses”.

Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists.

However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century’s end, most textbooks on physiology and psychology were presenting pain specificity as fact.

Who founded pain?

Abstract – Pain management in the United States reflects attitudes to those in pain. Increased numbers of disabled veterans in the 1940s to 1960s led to an increased focus on pain and its treatment. The view of the person in pain has moved back and forth between a physiological construct to an individual with pain where perception may be related to social, emotional, and cultural factors.

Conceptually, pain has both a medical basis and a political context, moving between, for example, objective evidence of disability due to pain and subjective concerns of malingering. In the 20th century, pain management became predominately pharmacologic. Perceptions of undertreatment led to increased use of opioids, at first for those with cancer-related pain and then later for noncancer pain without the multidimensional care that was intended.

The increased use was related to exaggerated claims in the medical literature and by the pharmaceutical industry, of a lack of addiction in the setting of noncancer pain for these medications—a claim that was subsequently found to be false and deliberatively deceptive; an epidemic of opioid prescribing began in the 1990s.

An alarming rise in deaths due to opioids has led to several efforts to decrease use, both in patients with noncancer conditions and in those with cancer and survivors of cancer. Keywords: Pain management in the United States, pain and disability in politics in the United States, political impact in the United States on pain management, opioid epidemic, opioid deaths, pain management in patients with cancer, cancer survivorship and pain management Between 1999 and 2016, more than 630 000 persons in the United States died from drug overdoses—most of these drug-related deaths were due to opioids prescribed for pain.1 From 1999 to 2010, overdose deaths due to opioid pain relievers increased continuously, a time known as the first wave of the opioid epidemic.

After this wave, the second and the third waves of opioid overdose deaths due to heroin and illicitly manufactured fentanyl (IMF), respectively, affected the United States significantly.1 – 6 There was an increase in deaths from 52 404 in 2015 to 72 000 deaths (provisional) by 2017.7 – 9 A recent suggested revision to the classification of prescription opioid-related deaths removes synthetic opioids (such as fentanyl) from this category to better characterize those deaths as, increasingly, from illicit opioids.

This reclassification has important implications for strategies to address the problem as we discuss under possible solutions.10 This article reviews the evolution of the understanding of pain and the impact of pain (initially with disability of WW II veterans as the proxy for the subjective symptom of pain) on the political, legal, and regulatory systems in the United States as a template for the increase in use of opioids in the past 2 decades.

Finally, we discuss current solutions to the opioid epidemic—guidelines, policies, monitoring and other approaches. Space does not permit an expansion of the sociological background—the article by Dasgupta 5 explores these causes of the rise in abuse of both illicit and prescription opioids.

Modern theories of pain began with Descartes in the mid-1600s with his theory of pain specificity.
A painful stimulus on the surface of the body was transmitted by a nerve through the spinal cord to a site in the brain where pain was perceived.11 – 15 This theory had several implications—pain was a physiologic concept that was seemingly straightforward, but left out were the emotional, cultural, or social modification of the message, and only one site in the brain processed pain input.

Most importantly, the body and the mind were separate in this conceptualization. The understanding of pain evolved over the next 3 centuries—metaphysical explanations and the influence of the church waned; suffering and psychological components were further downplayed; however, by the 1900s, the notion of suffering and the psychological component again was acknowledged.

Finally, the concept of modulation of the pain message assumed more importance with the 1968 publication of the Gate Control Theory of Pain.13 The further evolution of this theory has helped reinsert components of suffering—psychological, spiritual, and cultural that were discounted over the past 4 centuries.

This theory was advanced in part due to the political and cultural ethos that was extant and evolving pari passu with the understanding of the mechanism of pain from a simple transmission along a defined pathway to modulation of the message by areas of the brain that respond to related factors such as culturally learned stoicism.15 The therapies for pain began to evolve in the United States in the middle of the 19th century with the development and use of morphine for injured Civil War soldiers.

In the late 1800s and early 1900s, there was reticence on the part of some physicians and some patients to use anesthetics and analgesics and instead to rely on nonpharmacologic measures. By the middle of the 1900s (with the return of the injured World War II soldiers), therapy was predominately pharmacologic, in part related to the same political and cultural ethos.16 Bourke 11 has chronicled stories of acute pain before the widespread use of anesthetic agents such as ether and chloroform, whose use began in the late 1840s, and later in injured soldiers and civilians in the Civil War era.

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A dilemma arose in former soldiers who continued to use morphine after the war. This usage for ongoing chronic pain lead to restrictions on morphine in the early part of the 1900s and heroin in the 1920s.14, 16 Usage of veteran’s services was modest before World War II.

Henry Beecher and John Bonica, both anesthesiologists after the war, chronicled that soldiers with severe and sometimes lethal wounds, denied pain, and focused on a return to their comrades on the battlefield. Others in obvious pain improved with the use of barbiturates to relieve anxiety. These observations led to a renewed acknowledgment of the role of psychological, cultural, and social (eg, bonding on the battlefield) factors.11, 12, 15 Continued pain after the war injury and after return to civilian life posed increasing challenges to US society, which were manifested in a dramatic rise in the number of disabled veterans and the need to provide services for them.

Wailoo documents the role that politics, both governmental and medical, played in decisions in the late 1940s and 1950s in the management of chronic pain and disability as its proxy. When the disability was due to the subjective symptom of pain, those who argued to believe the individual such as Beecher and Bonica were confronted by those seeking to quantify the problem for either monetary compensation or deny the existence of the problem.

How effective is the WHO analgesic ladder?

Conclusion – Use of the SF-MPQ for pain assessment and the WHO three-step analgesic ladder approach for pain management in hemodialysis patients led to effective pain relief in 96% of patients. Because older patients had higher posttreatment pain scores and adverse effects from treatment, they will need more careful management to achieve the same results as younger patients. Figure 1: The World Health Organization three-step analgesic ladder modified to exclude drugs unsafe in renal failure. Patients were treated with medications in step 1 when they rated their pain as a 1 to 4 on a 10-point scale. Patients were treated with medications in step 2 when they rated their pain as a 5 or 6 on a 10-point scale. Figure 2: Study participants. A total of 143 of 172 potentially eligible hemodialysis patients met inclusion criteria: 78 (54%) patients reported pain; 45 (58% of the patients in pain) agreed to participate in the study. Figure 3: Mean pretreatment pain score by gender, age, and race. Mean pretreatment scores for all groups were in the severe range (7.4 to 8.0). There was no difference in mean pretreatment pain score on the basis of gender, age, or race. The bars depict mean score ± 1 SD. Figure 4: Mean pre- and posttreatment pain scores by type of pain. Mean pretreatment scores for patients who reported neuropathic and nociceptive pain both were in the severe range (8.1 ± 1.2 versus 7.4 ± 1.2; P = 0.11). There was comparable reduction in pain scores for both groups to the mild range (1.5 ± 1.1 versus 1.8 ± 1.5, P = 0.524). The bars depict mean score ± 1 SD. Figure 5: Response to pain treatment by age. Both age groups had reduction of their mean pain scores from the severe to the mild range. Patients who were younger than 65 yr had a significantly lower posttreatment pain score than those who were 65 yr and older (0.94 ± 0.93 versus 2.1 ± 1.4, P = 0.003).

What is the hierarchy of pain?

How does chronic pain relate to our mental health? – Unfortunately, chronic pain affects every part of our being – mentally and physically. The physical turmoil is usually what you think about when you first think of chronic pain. Pain makes it difficult to complete even daily tasks.

Psychologist Abraham Maslow created a hierarchy of needs that is the basis for human motivation.
The hierarchy starts with physiological needs, then safety, love and belonging, esteem, and self-actualization.
If you have chronic pain, it may prevent you from being able to meet all of your needs.
If you are unable to maintain a social life, self-esteem, relationships, hobbies, and work-life you will have an increased risk for extra stress and depression.

But the good news is, there are ways that you can manage your chronic pain on both a physical and psychological level.

What is the reverse pain ladder?

Pain is an individual experience influenced by the patient’s perception, history and expression of pain, e.g. ability to cope, mental wellbeing, previous experience of pain, communication skills, family or cultural background. Key questions for the patient when assessing pain are:

How severe is the pain and what does it feel like? Where does the pain occur, how often is it occurring, and is it radiating? When did the pain start? What alleviates the pain? What makes the pain worse?

A verbal descriptor, e.g. none, mild, moderate, severe or excruciating, or a numerical scale, e.g. zero (none) to ten (worst pain imaginable), are useful methods to quantify the level of pain, and how it is progressing. A visual tool such as the Faces Pain Scale may be more appropriate for children, people with cognitive difficulties and people who do not speak English.1 The Faces Pain Scale for children is available from: https://www.iasp-pain.org/Education/Content.aspx?ItemNumber=1519 The primary aim of acute pain management * is to provide treatment that reduces the patient’s pain, with minimal adverse effects, while allowing them to maintain function.

A secondary aim is to prevent acute pain from progressing to chronic pain.
After treating the underlying cause of the pain, where possible It is important that patients have a realistic expectation of what their pain management strategy will achieve – an analgesic regimen that removes all experience of pain is usually not possible.

Discuss with the patient that analgesic medicines will reduce their amount of pain to a manageable level, although it may take some time initially to get the dose right. The effectiveness of an analgesic regimen can be attributed to not only the pharmacological effects of the medicine, but also to the awareness that pain is being treated and the routine of taking medicines (a placebo component).1 Patients can be reassured that their pain is expected to improve with time (try to give a likely duration for this) and their requirements for medicines will decrease.

Explaining that medicines for acute pain are for short-term use only and setting a plan for decreasing doses and strengths can help to avoid inappropriate use of opioids and acute pain becoming chronic.
Anxiety, depression, stress, insomnia and catastrophising increase the likelihood that acute pain will become chronic, particularly post-surgery; patients who display any of these features will require additional reassurance that their pain is being managed and is expected to resolve.

For patients with acute low back pain in particular, psychosocial and occupational factors, e.g. dissatisfaction with their job, are associated with progression from acute to chronic pain; identify factors early for intervention. Regular assessment of pain improves management and outcomes Patients prescribed analgesics for acute pain should be followed up regularly to ensure that their pain is resolving and their medicine requirements are diminishing.

Pain that is unable to be managed or that increases in intensity warrants consideration of other causes, e.g. surgical complication, infection or an alternative diagnosis, e.g. neuropathic pain. A pharmacological treatment regimen for acute pain can be based on the WHO analgesic ladder The World Health Organisation (WHO) analgesic ladder is widely accepted for the management of nociceptive pain.2 In patients with acute pain the ladder is generally used in reverse, e.g.

in severe acute pain, begin with morphine at Step 3, then as the pain resolves, reduce to codeine at Step 2, and continue with paracetamol at Step 1 until pain is negligible ( Figure 1 ).3 Adjuvant treatments, e.g. physiotherapy or non-analgesic medicines, are continued throughout treatment, as appropriate. Figure 1: The WHO analgesic ladder of medicines Response to analgesia is variable, so an analgesic regimen needs to be individualised There are many reasons why individual patients will respond differently to a standard dose of an opioid, including their level of pain, renal function, co-morbidities, co-prescribed medicines and genetics.

CYP2D6 polymorphisms, i.e. people who are fast or slow metabolisers of CYP2D6 enzymes, affect plasma concentrations of codeine and tramadol (and to a lesser extent, oxycodone) and either increase adverse effects or decrease effectiveness. Therefore, doses of opioids should be individualised, within recommended ranges, according to the patient’s particular clinical circumstances.

In a primary care setting, oral forms of analgesia are preferred and it is usually recommended to begin with regular use of short-acting preparations, while establishing opioid requirements, then consider switching to a controlled release formulation.3, 4 Consider appropriate dose reductions in elderly or frail patients, but do not under treat pain.

Multi-modal analgesia improves acute pain management Multi-modal analgesia refers to the concurrent use of analgesics with different modes of action, e.g. paracetamol or a NSAID used with an opioid. Multi-modal regimens result in improved pain relief, compared to monotherapy, and consequently a reduction in the opioid dose required, as well as a reduced risk of adverse effects.1, 5 Multi-modal analgesia also provides patients with reassurance that they will have pain relief as treatment is de-escalated.

For example, a patient is initially prescribed codeine, paracetamol and ibuprofen; they are advised to continue treatment with paracetamol and ibuprofen while the dose of codeine is reduced and then withdrawn, then the dose of the NSAID is reduced and withdrawn, and finally, when the pain is considered to be negligible the paracetamol is withdrawn.

Consider the need for additional medicines such as laxatives, anti-nausea and gastro-protection A laxative should almost always be prescribed if a patient is going to be taking opioids for more than a few days. Nausea and vomiting associated with opioids is usually dose-related. If adverse effects are intolerable, and pain relief is not adequate if the dose of opioid is lowered or the patient is switched to a different opioid, then consider adding an anti-nausea medicine such as prochlorperazine, cyclizine or metoclopramide.

A proton pump inhibitor may be required for patients prescribed a NSAID who are at risk of gastrointestinal complications. Additional medicines may be required if there is a neuropathic component to the patient’s pain, e.g. tricyclic antidepressants (TCAs), gabapentin or pregabalin.

For further information see: “Managing patients with neuropathic pain” www.bpac.org.nz/BPJ/2016/May/pain.aspx Provide patients with a written analgesia plan, accompanied by a verbal explanation of the instructions. A pain management regimen often consists of multiple medicines that have to be administered at different times and at different doses.

Patients or their caregivers need to be able to clearly understand their plan, keep track of their medicines and know what they have taken, when they can take the next dose, and when to stop. A written analgesia plan ensures that patients know their medicine regimen, and it can help to minimise medicine errors and optimise pain management with regular, adequate dosing.

The regular dose, frequency and dosing interval for each medicine, including extra doses that could be taken for breakthrough pain Adverse effects that may occur and how these should be managed, e.g. reducing the dose, taking with food or seeking medical advice The likely timeframe for pain resolution and instructions on how to reduce the dose and stop medicines as pain improves

Depending on the specific clinical circumstances, non-pharmacological treatments, e.g. elevation of an injured leg, and treatment goals, e.g. walking to the letterbox at the end of the first week following surgery, could also be included in the patient’s plan.

An example of an analgesic plan is available here: www.guild.org.au/_data/assets/pdf_file/0017/6209/patient-resource-my-pain-management-plan-nps-medicines-wise4e0a9a33c06d6d6b9691ff000026bd16.pdf Depending on the cause for the pain, physical interventions such as exercise, physiotherapy and heat application may be appropriate alongside the pharmacological regimen A variety of non-pharmacological interventions may be beneficial for patients with acute pain, depending on the cause.

For example: 1

Referral to a physiotherapist following a soft tissue helps to maintain movement, slow muscle de-conditioning and may avoid further injury Exercise, staying active and application of heat can improve outcomes in acute low back pain Yoga may improve back pain and enhance mindfulness 6 Massage may improve sleep in patients with musculoskeletal pain A heat pack on the lateral abdomen or lower back may provide relief for patients with renal colic 7

There is limited evidence to support the use of transcutaneous electrical nerve stimulation (TENS) or acupuncture in the management of acute pain, however, as there are significant placebo affects associated with pain interventions some patients may find these to be effective.8 Psychological distraction techniques such as listening to music can lead to better pain management outcomes There is a significant psychological component to managing pain.

What is the safest pain medication to take?

Acetaminophen – Acetaminophen is usually recommended as a first line treatment for mild to moderate pain. It might be taken for pain due to a skin injury, headache, or conditions that affect the muscles and bones. Acetaminophen is often prescribed to help manage osteoarthritis and back pain. It also may be combined with opioids to reduce the amount of opioid needed.

Generic (brand) names. Acetaminophen (Tylenol, others).
How it works. Acetaminophen is thought to block the production of prostaglandins in the central nervous system. Prostaglandins are hormonelike substances that are involved in pain and inflammation. Unlike NSAIDs, acetaminophen doesn’t target inflammation at the site of injury — only pain.
Benefits and risks. Acetaminophen is generally considered safer than other pain relievers. It doesn’t cause side effects such as stomach pain and bleeding. However, taking more than the recommended dose or taking acetaminophen with alcohol increases the risk of kidney damage and liver failure over time.
Bottom line. Acetaminophen is generally a safe option to try first for many types of pain, including chronic pain. Ask your health care provider for guidance about other medications to avoid while taking acetaminophen. Acetaminophen is not as effective as NSAIDs for the treatment of knee and hip pain related to osteoarthritis.

Who created the 1 10 pain scale?

Current Use – Through the years, the Wong-Baker FACES® Pain Rating Scale grew in popularity and use around the world. Donna’s books, published by Elsevier Inc., were a significant reason for the wide-spread use. Also during this time, Donna earned her PhD.

Another Wong-Baker FACES Foundation board member, Pam DiVito-Thomas, PhD, RN, CNE and Dr.
Donna Wong spent 5 years on an international and longitudinal study on three continents.
That data was collated, but never written.
We believed the data had been lost, until recently, when Dr.
DiVito-Thomas found it on a flash drive! In 2003, former board member, Dr.

Kristie Nix, joined with Dr. Donna Wong to research the use of the pain scale with adults. Sadly, Dr. Donna Wong died in May of 2008, but her work lives on through the Wong-Baker FACES® Pain Rating Scale, her students and mentees, and her lifetime contribution in pediatric nursing, including her textbooks and countless articles.

You may read more about Donna Wong in the About Us section of this website. Drs. Ting and Donna Wong’s daughter, Dr. Nina Wong Morrissette, an anesthesiologist, wife, and mother of two children, has joined the Wong-Baker FACES Foundation board. In 2009, Connie Baker began the Wong-Baker FACES Foundation to continue the work of protecting the integrity of the scale, as well as promoting excellence in pain care.

The Wong-Baker FACES® Pain Rating Scale has a registered copyright and trademark. People from nearly all countries in the world have visited this website. The scale is translated into over 60 languages, and the list is growing. The FACES Scale was created with children for children and it remains widely used.

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The scale is supported by years of research, and it continues to be used in study around the world. However, time shows that the scale is valid for use with people of ages three and older, not limited to children. Other investigators have used the faces scale with adults, especially the elderly, with successful results.

The cartoon-type faces scale avoids gender, age, and racial biases. Connie Baker offers interviews with experts in pain care and atraumatic care on her podcast, FACES of Pain Care. She invites you to visit the page and subscribe to FACES of Pain Care,

Who defined pain?

Criticisms of the definition and note: – Criticisms of the IASP definition have included that it is “Cartesian,” ignoring the multiplicity of mind-body interactions, and that it neglects “the ethical dimensions of pain” and does not adequately address pain in disempowered and neglected populations, such as neonates and the elderly,

It has been argued that the current definition emphasizes verbal self-report at the expense of nonverbal behaviors that may provide vital information, especially in non-human animals and humans with impaired cognition or language skills,
A concern expressed recently about the current definition was that it excluded cognitive and social factors that are integral to the experience of pain,

In addition, the term “unpleasant” has been debated as potentially trivializing the severe pain and suffering associated with many acute and chronic clinical pain states and fails to capture “the full range of words that could be used to describe the experience” and its associated suffering,

Finally, it has also been argued that pain is more than a symptom, that chronic pain may be a disease with its own clinical course, and hence the definition should reflect this perspective. In recent years, several alternate definitions have been proposed ( Table 1 ). Williams and Craig defined pain as “a distressing experience associated with actual or potential tissue damage with sensory, emotional, cognitive and social components.” Cohen et al.

offered the following revised definition: “Pain is a mutually recognizable somatic experience that reflects a person’s apprehension of threat to their bodily or existential integrity.” Other definitions and modifications to the IASP definition have been proposed by Wright and Aydede ( Table 1 ).

Who is the father of pain killer?

From Wikipedia, the free encyclopedia

John Bonica
Born	John Joseph Bonica February 16, 1917 Filicudi, Sicily, Italy
Died	August 15, 1994 (aged 77) Rochester, Minnesota, United States
Nationality	Sicilian
Citizenship	Italian / American
Scientific career
Fields	Anesthesiology / Pain Medicine

John Joseph Bonica (February 16, 1917 – August 15, 1994) was a Sicilian American anesthesiologist and professional wrestler known as the founding father of the discipline of pain medicine,

What is the original pain theory?

History and legacy – The firing of the projection neuron determines pain. The inhibitory interneuron decreases the chances that the projection neuron will fire. Firing of C fibers inhibits the inhibitory interneuron (indirectly), increasing the chances that the projection neuron will fire. Firing of the Aβ fibers activates the inhibitory interneuron, reducing the chances that the projection neuron will fire, even in the presence of a firing nociceptive fiber. Gate control theory asserts that activation of nerves which do not transmit pain signals, called nonnociceptive fibers, can interfere with signals from pain fibers, thereby inhibiting pain.

Afferent pain-receptive nerves, those that bring signals to the brain, comprise at least two kinds of fibers – a fast, relatively thick, myelinated “Aδ” fiber that carries messages quickly with intense pain, and a small, unmyelinated, slow “C” fiber that carries the longer-term throbbing and chronic pain,

Large-diameter Aβ fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibers. When it was first proposed in 1965, the theory was met with considerable skepticism. Despite having to undergo several modifications, its basic conception remains unchanged.

Ronald Melzack and Patrick Wall introduced their “gate control” theory of pain in the 1965 Science article “Pain Mechanisms: A New Theory”.
The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the spinal cord: transmission cells that carry the pain signal up to the brain, and inhibitory interneurons that impede transmission cell activity.

Activity in both thin and large diameter fibers excites transmission cells. Thin fiber activity impedes the inhibitory cells (tending to allow the transmission cell to fire) and large diameter fiber activity excites the inhibitory cells (tending to inhibit transmission cell activity).

So, the more large fiber (touch, pressure, vibration) activity relative to thin fiber activity at the inhibitory cell, the less pain is felt.
The authors had drawn a neural “circuit diagram” to explain why we rub a smack.
They pictured not only a signal traveling from the site of injury to the inhibitory and transmission cells and up the spinal cord to the brain, but also a signal traveling from the site of injury directly up the cord to the brain (bypassing the inhibitory and transmission cells) where, depending on the state of the brain, it may trigger a signal back down the spinal cord to modulate inhibitory cell activity (and so pain intensity).

The theory offered a physiological explanation for the previously observed effect of psychology on pain perception. In 1968, three years after the introduction of the gate control theory, Ronald Melzack concluded that pain is a multidimensional complex with numerous sensory, affective, cognitive, and evaluative components.

Melzack’s description has been adapted by the International Association for the Study of Pain in a contemporary definition of pain. Despite flaws in its presentation of neural architecture, the theory of gate control is currently the only theory that most accurately accounts for the physical and psychological aspects of pain.

The gate control theory attempted to end a century-old debate about whether pain is represented by specific neural elements ( specificity theory ) or by patterned activity ( pattern theory ) within a convergent somatosensory subsystem. Although it is now considered to be oversimplified with flaws in the presentation of neural architecture, the gate control theory spurred many studies in pain research and significantly advanced our understanding of pain.

What is the original pain theory?

Issues of Concern – Intensity Theory The theory goes back to the Athenian philosopher Plato ( c,428 to 347 B.C.) who in his work Timaeus, defined pain not as a unique experience, but as an ’emotion’ that occurs when the stimulus is intense and lasting.

Centuries later, we are aware that especially chronic pain represents a dynamic experience, profoundly changeable in a spatial-temporal manner.
A series of experiments, conducted during the nineteenth century, sought to establish the scientific basis of the theory.
These investigations, based on the tactile stimulation and impulses of other nature such as electrical stimulations, provided important information concerning the threshold for tactile perceptions and the role of the dorsal horn neurons in the transmission/processing of pain.

Cartesian Dualistic Theory The oldest explanation for why pain manifested in specific populations was rooted in religious beliefs. Throughout history, religious ideologies have had a substantial influence on people’s thoughts and actions. As a result, the majority of people believed that pain was the consequence of committing immoral acts.

There was also a belief that the suffering they endured was the individual’s way to repent for these sins. Although this belief remained popular up until the nineteenth century, this was not due to the lack of other available theories. One of the first alternative scientific pain theories was bravely introduced in 1644 by the French philosopher Renee Descartes (1596-1650).

This theory has the name in current literature as the Cartesian dualism theory of pain. The dualism theory of pain hypothesized that pain was a mutually exclusive phenomenon. Pain could be a result of physical injury or psychological injury. However, the two types of injury did not influence each other, and at no point were they to combine and create a synergistic effect on pain, hence making pain a mutually exclusive entity.

In an attempt to placate the church, Descartes also included in his theory the idea that pain has a connection to the soul. He claimed that his research uncovered that the soul of pain was in the pineal gland, consequentially designating the brain as the moderator of painful sensations. The dualistic approach to pain theory fails to account for many factors that are known to contribute to pain today.

Furthermore, it lacks an explanation as to why no two chronic pain patients have the same experience with pain even if they had similar injuries. Despite these shortcomings, it still provided future researchers with a solid foundation to continue expanding the scientific understanding of the intricate phenomenon of pain.

Specificity Theory Many scientists continued to do research long after Descartes proposed the dualistic theory of pain. However, it wasn’t until 1811 that another well-known pain theory came onto the scene. This theory, initially presented by Charles Bell (1774–1842), is referred to as the specificity theory.

This theory is similar to Descartes’ dualistic approach to pain in the way that it delineates different types of sensations to different pathways. In addition to the identification of specific pathways for different sensory inputs, Bell also postulated that the brain was not the homogenous object that Descartes believed it was, but instead a complex structure with various components.

Scientists and philosophers alike spent the next century and a half further developing the specificity theory.
One of the many contributors to this theory was Johannes Muller.
In the mid-1800s, Muller published in the Manual of Physiology that individual sensations were the result of specific energy experienced at certain receptors.

Furthermore, Muller believed that there was an infinite number of receptors in the skin, and this surplus of receptors accounted for the ability of an individual to discriminate between different sensations. In 1894, Maximillian von Frey made another critical addition to the specificity theory that served to advance the concept.

This contribution to the theory was the discovery of the four separate somatosensory modalities found throughout the body. These sensations include cold, pain, heat, and touch. This concept correlates well with previous research done regarding this theory of pain, which served to reiterate the presence of distinct pathways for different sensations.

Although this theory and the research surrounding it provided significant advancement to the understanding of pain, it still fails to account for factors other than those of physical nature that result in the sensation of pain. Much like the dualistic approach to pain, this theory also lacks an explanation for why sometimes pain persists long after the healing of the initial injury.

This incomplete nature of the specificity theory regarding pain etiology necessitated additional theories and continued research.
Pattern Theory Following the specificity theory, there were a handful of other philosophies introduced regarding the sensation of pain.
Of these philosophies, the pattern theory of pain has the greatest coverage in the scientific literature.

The American psychologist John Paul Nafe (1888-1970) presented this theory in 1929. The ideas contained in the pattern theory were directly opposite to the ideas suggested in the Specificity theory in regards to sensation. Nafe indicated that there are no separate receptors for each of the four sensory modalities.

Instead, he suggested that each sensation relays a specific pattern or sequence of signals to the brain.
The brain then takes this pattern and deciphers it.
Depending on which pattern the brain reads, correlates with the sensation felt.
At the time of its introduction, the pattern theory gained significant popularity among many researchers.

However, through further research and the discovery of unique receptors for each type of sensation, it can be stated with certainty, that this theory is an inaccurate explanation for how we feel pain. Gate Control Theory In 1965, Patrick David Wall (1925–2001) and Ronald Melzack announced the first theory that viewed pain through a mind-body perspective.

This theory became known as the gate control theory. Melzack and Wall’s new theory partially supported both of the two previous theories of pain but also presented more knowledge to advance the understanding of pain further. The gate control theory of pain states that when a stimulus gets sent to the brain, it must first travel to three locations within the spinal cord.

These include the cells within the substantia gelatinosa in the dorsal horn, the fibers in the dorsal column, and the transmission cells which are located in the dorsal horn as well. The substantia gelatinosa of the spinal cord’s dorsal horn serves to modulate the signals that get through, acting similar to a “gate” for information traveling to the brain.

The sensation of pain that an individual feels is the result of the complex interaction among these three components of the spinal cord. Simply stated, when the “gate” closes, the brain does not receive the information that is coming from the periphery to the spinal cord. However, when the signal traveling to the spinal cord reaches a certain level of intensity, the “gate” opens.

Once the gate is open, the signal can travel to the brain where it is processed, and the individual proceeds to feel pain. The information mentioned above accounts for the physical component of pain, but as stated earlier, the Gate Control Theory was one of the first to acknowledge that psychological factors contributed to pain as well.

In their original study, Melzack and Wall suggested that in addition to the control provided by the substantia gelatinosa, there was an additional control mechanism located in cortical regions of the brain.
In more recent times, researchers have postulated that these cortical control centers are responsible for the effects of cognitive and emotional factors on the pain experienced.

Current research has also suggested that a negative state of mind serves to amplify the intensity of the signals sent to the brain as well. For example, somebody who is depressed has a “gate” that is open more often, allowing more signals to get through, increasing the probability that an individual will experience pain from an otherwise normal stimulus.

Also, there are reports that certain unhealthy lifestyle choices will also result in an “open gate,” which in turn leads to pain that is disproportionate to the stimulus. The gate control theory has proven to be one of the most significant contributions to the study of pain throughout history. The concepts that Melzack and Wall introduced to the study of pain are still utilized by researchers today.

Even though this theory initiated the idea that pain wasn’t solely a result of physical injury but rather a complex experience, influenced by cognitive and emotional factors, there was still additional research necessary to comprehend the mechanisms and etiology of pain completely.

This need precipitated the introduction of the following two philosophies regarding pain.
Neuromatrix Model Almost thirty years after introducing the gate control theory of pain, Ronald Melzack introduced another model that contributed to the explanation of how and why people feel pain.
Until the mid-1900s, most theories of pain implied that this experience was exclusively due to an injury that had occurred somewhere in the body.

The thinking was that if an individual suffered an injury, whether it be through trauma, infection, or disease, a signal would transmit to the brain which would, in turn, result in the sensation of pain. Although Melzack had contributed to these previous theories, it was his exposure to amputees that were experiencing phantom limb pain in well-healed areas that prompted his inquiry into this more accurate philosophy of pain.

The theory he proposed is known as the neuromatrix model of pain.
This philosophy suggests that it is the central nervous system that is responsible for eliciting painful sensations rather than the periphery.
The neuromatrix model denotes that there are four components within the central nervous system responsible for creating pain.

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The four components are the “body-self neuromatrix, the cyclic processing, and synthesis of signals, the sentinel neural hub, and the activation of the neuromatrix.” According to Melzack, the neuromatrix consists of multiple areas within the central nervous system that contribute to the signal, which allows for the feeling of pain.

These areas include the spinal cord, brain stem and thalamus, limbic system, insular cortex, somatosensory cortex, motor cortex, and prefrontal cortex.
The signal that these areas of the central nervous system work together to create is responsible for allowing an individual to feel pain, and he referred to as the “neurosignature.” Furthermore, this theory states that input coming in from the periphery can initiate or influence the neurosignature, but these peripheral signals cannot create a neurosignature of their own.

This idea that peripheral signals can alter the neurosignature is an important concept when considering the effect that nonphysical factors have on an individual’s experience with pain. Melzack’s theory claimed that not only are there specific neurosignatures that elicit certain sensations, but when there is an alteration in a certain signal, this allows for memory formation of these particular experiences.

If the same circumstances occur again in the future, it is this memory that allows for the same sensation to be felt. In addition to the hypothesis that pain was a product of different patterns of signals from the central nervous system, the neuromatrix model continued to elaborate on the idea that was initially brought forward in the gate control theory, that pain can be affected not only by physical factors but by cognitive and emotional factors.

Melzack suggested that hyperactivity of the stress response has a direct effect on pain. Hyperactivity of the stress response is when an individual exposed to increased levels of stress experiences a higher level of pain. Taking all of these claims into consideration, it is evident that pain is a complex issue that cannot be accounted for by physical factors alone.

Even though the neuromatrix model further established the idea that pain gets influenced by cognitive and emotional factors as well as physical factors, it still fails to account for social constructs of pain.
Therefore, a new theory of pain must be utilized to appropriately explain the mechanism behind pain and why each individual’s experience with pain is unique.

Biopsychosocial Model The biopsychosocial model provides the most comprehensive explanation behind the etiology of pain. This specific theory of pain hypothesizes that pain is the result of complex interactions between biological, psychological, and sociological factors, and any theory which fails to include all of these three constructs of pain, fails to provide an accurate explanation for why an individual is experiencing pain.

Although the term biopsychosocial was not introduced until 1954 by Roy Grinker (1900-1993), a neurologist and psychologist, there have been many physicians who had considered the utility of using such a model to approach the management of a patient’s pain long before this. One of the most prominent physicians who utilized this more comprehensive approach to pain was John Joseph Bonica (1917-1994), a Sicilian American anesthesiologist at Madigan Army Hospital, known as the founding father of the discipline of pain medicine.

In the 1940s, Bonica was caring for many patients who had returned home from World War II and were now experiencing debilitating pain due to injuries they had suffered in the war. He had recognized that the pain these wounded soldiers were experiencing was rather complex and not easily managed.

This situation led him to propose that to adequately manage these patients, physicians needed to create interprofessional pain clinics comprising multiple disciplines. At this moment in history, there was little support for the idea that pain was more than just the result of an injury, and Bonica was relatively unsuccessful in establishing these clinics.

It wasn’t until 1977 that the biopsychosocial model was scientifically suggested as an explanation for the etiology of some medical conditions. George Engle claimed that to treat disease adequately, one must consider multidimensional concepts and manage the whole patient instead of focusing on a single issue.

This methodology takes into account that the human body cannot be divided into separate categories when considering treatment options.
Instead, it is beneficial to acknowledge the fact that illness and disease are the results of complex interactions between biological, psychological, and sociological factors, and they all affect an individual’s physical and mental well-being.

Although Bonica had technically been the first physician to comprehend the importance of using a biopsychosocial approach to pain, John D. Loeser, another anesthesiologist, has been credited as the first person to use this model in association with pain.

Loeser suggested that four elements need to be taken into consideration when evaluating a patient with pain.
These elements include nociception, pain, suffering, and pain behaviors.
Nociception is the signal that is sent to the brain from the periphery to alert the body that there is some degree of injury or tissue damage.

Pain, on the other hand, is the subjective experience that occurs after the brain has processed the nociceptive input. The last two components of pain that merit consideration is suffering and pain behaviors. The thinking is that suffering is an individual’s emotional response to the nociceptive signals and that pain behaviors are the actions that people carry out in response to the experience of pain.

Both of these can be either conscious or subconscious. Loeser’s four elements of pain account for the biological, psychological, and sociological factors that can create or influence an individual’s experience with pain. Failing to consider any one of these four elements when determining the cause or establishing a management plan could be a consideration as inadequate assessment or care.

With a better understanding of what is causing a patient to experience pain, the doctor is provided with a more accurate foundation to begin formulating a treatment plan. Loeser’s findings prove that the Biopsychosocial Model of pain offers the most comprehensive philosophy and provides the framework that is needed to start appropriate therapy to manage patients with chronic pain adequately.

What is pain real name before death?

What Is Pain’s True Identity in Naruto – If you have watched Naruto Shippuden already, you will know Pain was an alias for Nagato, who belonged to the Uzumaki Clan, Behind the six paths of Pain, there was just one man all along, and his real identity was ” Nagato Uzumaki,” After certain soul-crushing life events, he picked up the alias of Pain and formed the infamous Akatsuki.

What is the reverse pain ladder?

A secondary aim is to prevent acute pain from progressing to chronic pain. * After treating the underlying cause of the pain, where possible It is important that patients have a realistic expectation of what their pain management strategy will achieve – an analgesic regimen that removes all experience of pain is usually not possible.

Explaining that medicines for acute pain are for short-term use only and setting a plan for decreasing doses and strengths can help to avoid inappropriate use of opioids and acute pain becoming chronic. Anxiety, depression, stress, insomnia and catastrophising increase the likelihood that acute pain will become chronic, particularly post-surgery; patients who display any of these features will require additional reassurance that their pain is being managed and is expected to resolve.

Pain that is unable to be managed or that increases in intensity warrants consideration of other causes, e.g.
Surgical complication, infection or an alternative diagnosis, e.g.
Neuropathic pain.
A pharmacological treatment regimen for acute pain can be based on the WHO analgesic ladder The World Health Organisation (WHO) analgesic ladder is widely accepted for the management of nociceptive pain.2 In patients with acute pain the ladder is generally used in reverse, e.g.

CYP2D6 polymorphisms, i.e.
People who are fast or slow metabolisers of CYP2D6 enzymes, affect plasma concentrations of codeine and tramadol (and to a lesser extent, oxycodone) and either increase adverse effects or decrease effectiveness.
Therefore, doses of opioids should be individualised, within recommended ranges, according to the patient’s particular clinical circumstances.

Consider the need for additional medicines such as laxatives, anti-nausea and gastro-protection A laxative should almost always be prescribed if a patient is going to be taking opioids for more than a few days. Nausea and vomiting associated with opioids is usually dose-related. If adverse effects are intolerable, and pain relief is not adequate if the dose of opioid is lowered or the patient is switched to a different opioid, then consider adding an anti-nausea medicine such as prochlorperazine, cyclizine or metoclopramide.

For further information see: “Managing patients with neuropathic pain” www.bpac.org.nz/BPJ/2016/May/pain.aspx Provide patients with a written analgesia plan, accompanied by a verbal explanation of the instructions. A pain management regimen often consists of multiple medicines that have to be administered at different times and at different doses.

An example of an analgesic plan is available here: www.guild.org.au/_data/assets/pdf_file/0017/6209/patient-resource-my-pain-management-plan-nps-medicines-wise4e0a9a33c06d6d6b9691ff000026bd16.pdf Depending on the cause for the pain, physical interventions such as exercise, physiotherapy and heat application may be appropriate alongside the pharmacological regimen A variety of non-pharmacological interventions may be beneficial for patients with acute pain, depending on the cause.

For example: 1

Who is pain master?

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