PubMed · 8197221
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G Bejeuhr. 1994. [Epibatidine].. https://doi.org/10.1002/pauz.19940230210
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Convincing evidence from preclinical studies demonstrates that cannabinoids can reduce pain responses in a range of inflammatory and neuropathic pain models. The anatomical and functional data reveal cannabinoid receptor-mediated analgesic actions operating at sites concerned with the transmission and processing of nociceptive signals in brain, spinal cord and the periphery. The precise signalling mechanisms by which cannabinoids produce analgesic effects at these sites remain unclear; however, significant clues point to cannabinoid modulation of the functions of neurone and immune cells that mediate nociceptive and inflammatory responses. Intracellular signalling mechanisms engaged by cannabinoid receptors-like the inhibition of calcium transients and adenylate cyclase, and pre-synaptic modulation of transmitter release-have been demonstrated in some of these cell types and are predicted to play a role in the analgesic effects of cannabinoids. In contrast, the clinical effectiveness of cannabinoids as analgesics is less clear. Progress in this area requires the development of cannabinoids with a more favourable therapeutic index than those currently available for human use, and the testing of their efficacy and side-effects in high-quality clinical trials.
The distribution of ion channels in neurons associated with pain pathways is becoming better understood. In particular, we now have insights into the molecular nature of the channels that are activated by tissue-damaging stimuli, as well as the mechanisms by which voltage-gated channels alter the sensitivity of peripheral neurons to change pain thresholds. This chapter details the evidence that individual channels may be associated with particular pain states, and describes genetic approaches to test the possible utility of targeting individual channels to treat pain.
Organized orthopaedic pain management is a major part of successful patient treatment. Therefore pain management should start before surgery. Patients need to be informed about the operation and the subsequent procedures. Clinical pain management is based on continuous pain documentation with pain as the fifth vital sign. Surgery should be minimally invasive bewaring a peripheral modulated nociceptive sensitization. In order to prevent chronic pain preemptive analgesia should be employed followed by an individually tailored regimen of post-operative analgesia. In consideration of the documented pain levels post-operative pain therapy consisting of a standing medication and a rescue medication should by adjusted daily. Due to the fact that the highest pain levels after surgery were reported within the first 48 h pain medication should be reduced in the ensuing days, again taking the documented pain levels into account. Supportive treatment approaches such as cryotherapy or transcutaneous electrical nerve stimulation (TENS) are useful in the post-operative period. Physiotherapy after surgery should be extended stepwise regarding the operative device and it is of particular importance to respect pain intensities. The post-hospital regimen for a continuous pain medication should be given to the orthopaedic specialist.