Central neurophysiological processing of joint pain on the basis of studies performed in normal animals and in models of experimental arthritis.
On the basis of anatomical and electrophysiological studies, this review summarizes first, the data dealing with the transmission of joint inputs in the central nervous system of normal animals at the spinal and supraspinal levels. It appears that in these conditions neuronal responses to mechanical noxious stimuli of the joints are relatively few and (or) weak. Second, in sharp contrast, the studies performed in polyarthritic rats have emphasized the profound changes in the activities (spontaneous firing and responsiveness) of the somatosensory neurones at various levels of the central nervous system (CNS), including the thalamus and primary somatosensory cortex; many were spontaneously active and a majority of them could be maximally activated by gentle mechanical stimuli applied to the inflamed joints. Although the change in the sensitivity of the peripheral mechanoreceptors has a major role in the modifications described in the CNS, additional observations have suggested a complex interaction between peripheral and central processes. On the basis of the recent data obtained in poly- and mono-arthritic animals; the following phenomena have been successively considered: the segmental and hetero-segmental "cross-talk" and their possible relationship with referred pain; the involvement of "new" neuronal populations as a possible basis of a selective system for joint pain; and the possible involvement of changes in the various control systems that normally modulate the nociceptive inputs at different levels of the CNS.
Guilbaud
G
G
Institut national de la santé et de la recherche médicale, U 161, Paris, France.
D000818:Animals; D001169:Arthritis, Experimental / Q000503:physiopathology*; D006801:Humans; D007592:Joint Diseases / Q000503:physiopathology*; D009420:Nervous System / Q000503:physiopathology*; D010146:Pain / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology