title: Cold and post-traumatic pain: modeling of the peripheral nerve message.
abstract: Hypersensitivity to cold is a relatively frequent sequel of peripheral nerve injuries but its mechanism is not well understood. We suggested that incomplete recovery of diameter of regenerated fibers is one of the factors involved in cold intolerance after nerve damage. Conduction velocity is correlated to fiber diameter, and is slowed down by cold. In normal subjects, cold does not desynchronize the volleys of sensory impulses sufficiently to change the intelligibility of the peripheral 'messages'. Sensory perceptions remain accurate although they acquire a characteristic numbness. On the other hand, post-traumatic reduction in fiber diameters causes a permanent distortion of the messages. We considered that when the distortion is severe, the resulting messages may be perceived by the centers as containing nociceptive components. We further hypothesized that, even in cases of moderate permanent distortion, cold acts by increasing the post-traumatic abnormalities of impulse synchronization. In winter, decompensation is observed when a threshold of desynchronization is reached. We constructed a model of peripheral nerve messages in an attempt to represent and quantitate the desynchronizations produced by cold and crush damage lesions in peripheral nerve messages. A number of parameters concerning fiber anatomy, exposure to cold, and type of nerve damage were taken into consideration. Four elementary types of desynchronization could be recognized by considering the times of arrival of pairs of impulses at the nervous centers. The difference between a normal and a distorted message could be expressed by eight variables. Thus, although our model was quite simple, a large amount of data was obtained and a preliminary statistical study was necessary in order to orient the final analysis. Then, we used factor analysis in an attempt to obtain a satisfactory interpretation of the data. The results indicated that peripheral desynchronization might explain, at least in part, the painful sensations experienced in winter by many patients after peripheral nerve injury.
authors.affiliation: National Institute of Mental Health, St Elizabeths Hospital, Washington DC, USA.
authors.forename: L
authors.initials: L
authors.lastname: de Medinaceli
authors.forename: J
authors.initials: J
authors.lastname: Hurpeau
authors.forename: M
authors.initials: M
authors.lastname: Merle
authors.forename: H
authors.initials: H
authors.lastname: Begorre
mesh_terms: D000700:Analgesics / Q000008:administration & dosage / Q000627:therapeutic use; D003080:Cold Temperature; D006801:Humans; D008954:Models, Biological; D010146:Pain / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D017933:Peripheral Nervous System / Q000293:injuries* / Q000503:physiopathology; D012646:Self Administration; D014947:Wounds and Injuries / Q000150:complications* / Q000503:physiopathology
chemical_list: D000700:Analgesics