Mechanisms of dynamic mechanical allodynia and dysesthesia in patients with peripheral and central neuropathic pain.

Eighteen patients with peripheral neuropathic pain (PNeP) and seven patients with central post-stroke pain (CPSP) all suffering from dynamic mechanical allodynia (DMA) in a limb were studied. From recent research it is reasonable to suggest that A-beta fibres constitute the peripheral substrate for DMA in patients with PNeP. The pathophysiological basis for DMA in patients with CPSP is unknown. It is clinically observed that some patients with neuropathic pain report variable intensity of DMA and volunteer that the phenomenon at times is only an unpleasant, i.e., dysesthetic sensation. The pathophysiological basis for dynamic mechanical dysesthesia (DMD) has never been addressed. Based on the aforementioned clinical observations we aimed at investigating if DMA is the hyperbole of DMD both mediated by A-beta fibres in the periphery. A compression/ischemia-induced (differential) nerve block in conjunction with repeated quantitative sensory testing of A-delta and C-fibre function using cold and warm stimuli was used to assess which nerve fibre population that contributes to DMA and DMD, respectively. During the nerve block there was a transition of DMA to DMD in all patients with PNeP and in 3/7 patients with CPSP. The rest of the patients lost DMA without transition to DMD. The transition or loss of DMA without transition occurred early and concurrently in time during the block and was paralleled by a continuous impairment of mainly A-beta fibre function. We therefore suggest DMA to be the hyperbole of DMD, the difference being the number of mechanoreceptive fibres having access to the nociceptive system.