title: [Neuronal mechanisms of chronic pain].
abstract: Until recently the paradigms of pain research were predominantly related to acute pain in humans and animals. Some 20 years ago the focus of basic and clinical research was shifted towards the mechanisms of chronic pain. Usually the nociceptors of our joints respond only to overload and lesions and thus serve protective functions. However, in case of a lasting pain condition mechanisms emerge in the nervous system that result in an increasing sensitivity of the neuronal pain system-these are the initial steps toward the process of pain chronicity. Inflammatory mediators including cytokines result in a dramatic enhancement of peripheral nervous system sensitivity. The ensuing plastic changes in the central neurotransmitter systems result in long term potentiation of synaptic transmission and may include adaptations in neuronal gene transcription. Interactions between the nervous and immune systems as well as learning processes may further wind up pain sensitivity. The tendency of perpetuation inherent to these processes contribute to pain chronicity-can this be halted by preventive treatment strategies?
authors.affiliation: Neuroscience and Pain Research Institute, Heidelberg. mzim@neuroscilett.de
authors.forename: M
authors.initials: M
authors.lastname: Zimmermann
mesh_terms: D000818:Animals; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D020078:Neurogenic Inflammation / Q000150:complications / Q000276:immunology / Q000503:physiopathology*; D009475:Neurons, Afferent; D009619:Nociceptors / Q000503:physiopathology*; D010146:Pain / Q000209:etiology / Q000503:physiopathology*; D010523:Peripheral Nervous System Diseases / Q000150:complications / Q000503:physiopathology*; D013116:Spinal Cord / Q000503:physiopathology*; D009435:Synaptic Transmission
chemical_list: D016207:Cytokines