The role of axonal excitability in neuropathic pain has gained new interest since mutations of the TTX sensitive sodium channel Nav 1.7 have been found to be linked to chronic painful diseases such as erythromelalgia or to insensitivity to pain. In awake human subjects axonal properties of C-fibers can be tested with the method of microneurography. Human C-fibers show activity dependent conduction velocity slowing ("slowing"), which can be examined with microneurography. In humans, the amount of slowing differs between different nociceptor classes and efferent sympathetic C-fibers. Mechano-responsive C-fibers (CMH) show less slowing than mechano-insensitive C-fibers (CMi). Sympathetic C-fibers have an intermediate slowing at low stimulation frequencies, however, when stimulated with 2 Hz stimulation frequency the slowing is terminated after one minute and after a phase of stable conduction velocity a slight speeding occurs. These differences are so stable and significantly linked to the sensory function of mechanosensitivity and sympathetic behaviour that human C-fibers could be classified only according to their slowing behaviour. Although the mechanisms influencing slowing behaviour are not yet completely understood, lately a study about rat dural afferents could show that activity dependent slowing is crucially dependent on the slow inactivation of sodium channels. Thus microneurography could provide access to sodium channel function in humans via scrutinizing slowing properties of their C-fibers. Unfortunately the role of different sodium channel subtypes, membrane potential and the differential expression of sodium channels on different nociceptor subclasses is not clear. Nevertheless microneurography could already provide information about sensory and axonal changes in patients with neuropathic pain. In patients with erythromelalgia spontaneously active C-fibers and sensitized C-fibers were observed. Only slight changes in slowing behaviour could be seen in the group analyses. However, in one of these patients specific changes in slowing behaviour were observed, which have similarity with the effect of injection of lidocaine in the skin near the nerve terminals suggesting sodium channel alterations. In conclusion, microneurography could be a tool to link the findings from genotyping and electrophysiology on a cellular level with the symptoms of patients with neuropathic pain by assessing axonal properties of human C-fiber endings.