| Literature DB >> 31914896 |
Kirsty Bannister1, Juliane Sachau2, Ralf Baron2, Anthony H Dickenson3.
Abstract
Neuropathic pain (NeP) can result from sources as varied as nerve compression, channelopathies, autoimmune disease, and incision. By identifying the neurobiological changes that underlie the pain state, it will be clinically possible to exploit mechanism-based therapeutics for maximum analgesic effect as diagnostic accuracy is optimized. Obtaining sufficient knowledge regarding the neuroadaptive alterations that occur in a particular NeP state will result in improved patient analgesia and a mechanism-based, as opposed to a disease-based, therapeutic approach to facilitate target identification. This will rely on comprehensive disease pathology insight; our knowledge is vastly improving due to continued forward and back translational preclinical and clinical research efforts. Here we discuss the clinical aspects of neuropathy and currently used drugs whose mechanisms of action are outlined alongside their clinical use. Finally, we consider sensory phenotypes, patient clusters, and predicting the efficacy of an analgesic for neuropathy.Entities:
Keywords: clinical targets; neurobiology; neuropathic pain; neuropathy; patient clusters; sensory phenotypes
Year: 2020 PMID: 31914896 DOI: 10.1146/annurev-pharmtox-010818-021524
Source DB: PubMed Journal: Annu Rev Pharmacol Toxicol ISSN: 0362-1642 Impact factor: 13.820