Dear Mr. Baptista, what is you refering to, sounds as quite interesting. I guess, you apply always DC current, in case of "monophasic currents" too. Also, in order to have comparable situations, you have to apply the same amperage in both cases, with the same arrangement and electrodes. Neuronal cells have a negative relaxing potential. Anodal i.e positive voltage will stimulate them, negative will cause more tranquility. These cells in the motor cortex can be seen as the source of the electric signal, the propagation. On the axon, the peripheral nerves can be seen more as distributors, as trasmission lines. The peripheral nerves have ions, literally positive (Na, K, Ca), although some negatives too (Cl). The action potential is already propagated elsewhere and they only transfer the pulse. Positive ions play the role of the electric signal carrier. When appying a negative voltage outside the axon, you motivate the positive ions, the signal travels faster and the excitability can be increased. I think this could be a possible explanation. However, you didn't mention if you applied positive voltage at the axon. Sorry if I didn't understand. Also I would like to know if you applied a voltage in the same direction with the axon (in parallel) or perpendicular to the axon. To put it in another way: What is the axon potential of the peripheral nerves in normal conditions, without stimulation (in the parallel direction)? Let us assume that the axon terminals are A and B, and the potential Vab>0 (Va>Vb). In this case when applying a positive voltage to A there should be an almost zero excitability (unless the voltage is too high). In contrast, supposing a negative voltage to A, there should be a stimulation. Usually (as I can recall) the head is more positive than the lower limbs. I guess, if you apply the same voltage to a perpendicular direction, you wont have the same results. 

Hi Abraho, 

I am honestly not quite sure, whether I understood your question correctly, since you are describing two different types of stimulation, but at least of two different kinds of interactions: Low current tDCS stimulation and some type (not further explained) of non-invasive peripheral stimulation. 

This sounds like comparing apples and pears... as we say here.

The tDCS is probably best described as a "de-tuning" of the neuron's intrinsic firing pattern - without actually "causing" action potentials. This falls under the terms STP/STD, dependent on the type of stimulation to the susceptible cells (orientation of cells to the electric field matters!) (see graphic "Weak_Stimulation" for a crude illustration)

See for further description: 

* Reato, D., A. Rahman, M. Bikson, and L.C. Parra Low-intensity electrical stimulation affects network dynamics by modulating population rate and spike timing. J Neurosci, 2010. 30(45): p. 15067-15079, 

*Froehlich, F. and D. McCormick, Endogenous electric fields may guide neocortical network activity. Neuron, 2010. 67(1): p. 129-143.

See for the orientation issue: 

*Krieg, T.D., F.S. Salinas, S. Narayana, P.T. Fox, and D.J. Mogul, PET-based confirmation of orientation sensitivity of TMS-induced cortical activation in humans. Brain Stimul, 2013. 6(6): p. 898-904

Now to the peripheral nerve stimulation: The procedure here is described by a theory from Frank Rattay 

(e.g.  *Rattay, F., L.P. Paredes, and R.N. Leao, Strength-duration relationship for intra- versus extracellular stimulation with microelectrodes. Neuroscience, 2012. 214: p. 1-13.

*Rattay, F., Analysis of models for external stimulation of axons. IEEE Trans Biomed Eng, 1986. BME-33(10): p. 974-977.) (see pic below artistically adjusted from Rattay 2012)

which essentially explains the triggering of action potentials ALONG the axon fibre. This is a completely different mechanism, as it is a completely different setting. 

So in essence, I do not think, that your "observation" state a paradoxon - there are different mechanisms involved. 

Cheers

uli