|
Mechanisms |
With
skin
anesthesia |
Without
skin
anesthesia |
1 |
Decreasing excitability of abnormally sensitized but intact sensory receptors in the skin [45] |
+ |
+ |
2 |
Inhibiting ectopic neural discharge in damaged afferents of the skin [46] |
+ |
+ |
3 |
Inhibiting ectopic neural discharge in primary afferents outside the skin (due to axoplasmic transport or systemic absorption) [46] |
+ |
+ |
4 |
Blockade of the propagation of pain signaling discharge (originated in intact or damaged nerve afferents in the skin) [47] |
+ |
– |
5 |
Blockade of all sensory input from the area of pain projection: pain cannot be projected and, therefore, felt [48] |
+ |
– |
6 |
Elimination of fiber interaction cross-talk or sensory inflow imbalance [49,50] |
+ |
– |
7 |
Elimination of central sensitization maintenance from a peripheral focus [44,48]
a) by inhibiting impulse generation
b) by blockade of impulse propagation |
+
+ |
+
– |
