PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11488183

[Future pain treatment].

L J Rygh·T H Fagerlund·F Svendsen
View original source ↗Export metadata ↓

Abstract

BACKGROUND: The recent rapid progress in pain research is due in large part to advances in genetics and cell and molecular biology. We now know that chronic pain (hypersensitivity due to inflammation or nerve injury) and acute nociceptive pain are different and must be treated accordingly. We will continue to reveal sophisticated mechanisms underlying different kinds of pain that can be targeted to inhibit nociceptive transmission and produce analgesia. METHODS: This review is based upon literature collected through the authors' own reading and through PubMed searches. New hopes for future pain treatments are discussed. Further, the impact of genetic factors on pain sensitivity and pain modulation are discussed, and conceivable therapeutic approaches based on genetic techniques are mentioned. RESULT: At the level of the peripheral nerve, many novel targets have recently been identified: the tetrodotoxin-resistant sodium channel, the vanilloid receptor and different calcium channels are very interesting. In the spinal cord, different approaches can be used: to either block excitatory input or to increase inhibitory control or to do both at the same time. The mechanisms for hypersensitivity are being identified and offer multiple possible targets for novel analgesics. INTERPRETATION: Many interesting targets for analgetics has emerged during that last few years, lending great hope for new and better (i.e. with less side effects) analgesic drugs in the future.

Explore related subjects

AnalgesiaAnalgesicsAnimalsGenetic TherapyHumansModels, NeurologicalNeuronal PlasticityNociceptorsPainPain ManagementPeripheral Nervous SystemPharmacogeneticsReceptors, N-Methyl-D-AspartateReceptors, OpioidResearchSpinal CordSynaptic TransmissionEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L J Rygh, T H Fagerlund, F Svendsen. 2001-06-20. [Future pain treatment].. https://pubmed.ncbi.nlm.nih.gov/11488183/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Capnography for procedural sedation and analgesia in the emergency department.

Although it is standard of care for patient safety monitoring in anesthesia, capnography is not routinely used for emergency department procedural sedation and analgesia. We discuss the use of capnography as a diagnostic monitoring modality for procedural sedation and analgesia, focusing on the physiology and interpretation of the CO2 waveform and recognition of normal, abnormal, and drug-induced ventilatory patterns.

Analgesia↗
PubMed2007

Interleukin-1 signaling modulates stress-induced analgesia.

Exposure to stressful stimuli is often accompanied by reduced pain sensitivity, termed "stress-induced analgesia" (SIA). In the present study, the hypothesis that interleukin-1 (IL-1) may play a modulatory role in SIA was examined. Two genetic mouse models impaired in IL-1-signaling and their wild-type (WT) controls were employed. Another group of C57 mice was acutely administered with IL-1 receptor antagonist (IL-1ra). Mice were exposed to 2min swim stress at one of three water temperatures: 32 degrees C (mild stress), 20-23 degrees C (moderate stress), or 15 degrees C (severe stress); and then tested for pain sensitivity using the hot-plate test. Corticosterone levels were assessed in separate groups of WT and mutant mice following exposure to the three types of stress. Mild stress induced significant analgesia in the two WT strains and saline-treated mice, but not in the mutant strains or the IL-1ra-treated mice. Similarly, mild stress induced significantly elevated corticosterone levels in WT mice, and blunted corticosterone response in mutant mice. In contrast, both WT and mutant strains, as well as IL-1ra-treated mice, displayed analgesic and corticosterone responses following moderate and severe stress. Interestingly, the analgesic response to moderate stress was markedly potentiated in the mutant strains, as compared with their WT controls. The present results support our previous findings that in the absence of IL-1, stress response to mild stress is noticeably diminished. However, the analgesic response to moderate stress is markedly potentiated in mice with impaired IL-1 signaling, corroborating the anti-analgesic role of IL-1 in several pain modulatory conditions, including SIA.

Analgesia↗
PubMed2007

Anticlotting drugs and regional anaesthetic and analgesic techniques: comparative update of the safety recommendations.

The wide use of anticlotting drugs by patients scheduled for surgery is a challenge for the anaesthesiologist when considering a regional anaesthesia technique. This practice seems safe if there is an appropriate management based on safety intervals established according to the pharmacology of the drug and the regional technique. Some anaesthesiology societies have published recommendations for the safe practice of regional anaesthesia with the simultaneous use of anticoagulants (heparin, low molecular weight heparins, oral anticoagulants (OA), fondaparinux and others) and antiplatelet agents (aspirin, clopidogrel, ticlopidine, argatroban and others). One of the most recent guidelines has been published by the Spanish Society of Anaesthesia and Critical Care. This article reviews these recommendations and compares them with others published in the last years. The recommendations are similar, but some interesting differences can be observed and need to be considered. A European consensus in this setting would probably be necessary.

Analgesia↗