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The levels of numbness, as indicated by normalized VFFs, paralleled the pattern of changes produced by paraesthesiae http://www.selleckchem.com/products/GDC-0941.html (Fig. 5B). During FNC, the mean tactile sensitivity deteriorated, followed by a gradual recovery with release of FNC. The changes in excitability parameters induced by FNC were reminiscent of previous studies that investigated the effects of ischaemia on nerve excitability (Han et al. 2008). In direct comparison to ischaemia, although the apparent reduction in threshold appeared smaller during FNC, the maximal threshold change achieved following release of compression was similar to that achieved previously with generalised limb ischaemia (Fig. 6A). Furthermore, the reduction in CSAP amplitude observed http://en.wikipedia.org/wiki/Diglyceride during compression was similar to that achieved with ischaemia (Fig. 6B), suggesting that the two manoeuvres achieved comparable effects on the axons over similar time period. Despite, the similar magnitude of CSAP reductions, the rates of recovery on release of the different interventions were clearly different. Direct comparison demonstrated that the rate of CSAP recovery was significantly faster following release of FNC (12.4 �� 2.1% min?1) when compared to ischaemia (3.6 �� 0.6% min?1; P http://www.selleckchem.com/products/AZD0530.html 5D; Han et al. 2008). In terms of explaining the biophysical basis for these differences in symptom generation, there appeared apparent coherence between the pattern of paraesthesiae and corresponding changes in SDTC. When directly correlated, the pattern of paraesthesiae generation during FNC closely followed the changes recorded in SDTC (Fig. 7). The present study has established the changes in axonal excitability that develop in human cutaneous afferents during and after a period of FNC, achieved using a novel nerve compression device. Changes in excitability induced by FNC were similar to those previously observed during ischaemia. As such, findings from the present series would suggest that there are similar biophysical mechanisms underlying the axonal changes observed during focal compression and more generalised limb ischaemia.