Selected pathobiological features and principles of pharmacological pain management

Abstract

Pain induced by inflammation and nerve injury arises from abnormal neural activity of primary afferent nociceptors in response to tissue damage, which causes long-term elevation of the sensitivity and responsiveness of spinal cord neurons. Inflammatory pain typically resolves following resolution of inflammation; however, nerve injury—either peripheral or central—may cause persistent neuropathic pain, which frequently manifests as hyperalgesia or allodynia. Neuralgias, malignant metastatic bone disease, and diabetic neuropathy are some of the conditions associated with severe, often unremitting chronic pain that is both physically and psychologically debilitating or disabling. Therefore, optimal pain management for patients with chronic neuropathic pain requires a multimodal approach that comprises pharmacological and psychological interventions. Non-opioid analgesics (e.g., paracetamol, aspirin, or other non-steroidal anti-inflammatory drugs) are first-line agents used in the treatment of mild-to-moderate acute pain, while opioids of increasing potency are indicated for the treatment of persistent, moderate-to-severe inflammatory pain. N-methyl D-aspartate receptor antagonists, antidepressants, anticonvulsants, or a combination of these should be considered for the treatment of chronic neuropathic pain. This review discusses the various neural signals that mediate acute and chronic pain, as well as the general principles of pain management.

Comparison of the Efficacy of Nonsteroidal Anti-Inflammatory Drugs and Opioids in the Treatment of Acute Renal Colic: A Systematic Review and Meta-Analysis

“…A total of 18 studies (Hetherington and Philp, 1986;Thompson et al, 1989;Oosterlinck et al, 1990;Sandhu et al, 1994;Cordell et al, 1996;Larkin et al, 1999;Safdar et al, 2006;Bektas et al, 2009;Serinken et al, 2012;Azizkhani et al, 2013;Ay et al, 2014;Masoumi et al, 2014;Pathan et al, 2016a;Zamanian et al, 2016;Al et al, 2018;Sotoodehnia et al, 2019;Rezaei et al, 2020) were included in this systematic review and meta-analysis, involving 3,121 participants who used NSAIDs or opioids for releasing pain. The primary outcome in this study-changes in the VAS at 0-30 min, showed the result of the nonsignificant difference between the NSAID and opioid groups, which is consistent with the study of Khammissa (2020). The conclusion of this outcome is consistent with previous studies (Das and Teece, 2006), but there is one article that clearly indicates significant advantage in favor of NSAIDs in the treatment of acute renal colic (Steinberg and Chang, 2016).…”

“…According to previous studies and this meta-analysis (Khammissa et al, 2020), the factors of analgesic effect of these two kinds of drugs are numerous and could be divided into two types, which involve the dose and routes of administration in patients, and the differences among individuals and environments (e.g., age, gender, and pain sensitivity).…”

Factors that influence the quality of life in neuropathic, musculoskeletal, and oncological pain

“…The neuropathic pain patients presented the lowest QoL values. This is due to the process of somatization of comorbidities 10,36 . Such association corroborates the difficulty in treating these patients, making them more susceptible to invasive pain control procedures, although they present a low success rate 37 .…”

Pain mitigation and management strategies for anti‐GD2 infusions: An expert consensus

“…The humanized anti‐GD2 mAb Hu14.18K322A, designed via a point mutation to reduce complement activity, was associated with reduced opioid requirements during infusion compared with dinutuximab, 16,17 with authors suggesting this is partially due to a reduction in complement‐dependent cytotoxicity 17 . Evidence also indicates that N‐methyl‐D‐aspartate receptor (NMDA‐R) activation may be involved: direct binding of mAbs to GD2 has been shown to activate the NMDA‐R on peripheral nerve fibers, 18,19 which is associated with hyperalgesia, neuropathic pain, and reduced opioid receptor functionality 20 …”

“…At analgesic doses, i.v. ketamine, given as a bolus dose in combination with lidocaine 29 or a continuous lower‐dose infusion, 20 has been successful in reducing anti‐GD2–associated pain 21,29 . However, given challenges in the routine use of ketamine at many institutions, it is generally reserved for patients in whom opioids are contraindicated or where opioids have provided insufficient analgesia.…”