ObjectiveIn neuropathic pain states, dynamic mechanical allodynia is mediated by large diameter AB-fibers. We test whether ongoing peripheral C-no-ciceptor input is necessary to maintain central changes hypothetically responsible for AB-mediated allodynia.Case reportA patient with long-standing diabetes mellitus demonstrated generalized signs of painless diabetic small fiber polyneuropathy. Following mechanical trauma, the patient additionally developed a typical neuropathic pain syndrome at the arm. Despite substantial impairment of cutaneous small fiber function, he complained of severe dynamic mechanical allodynia confined to a forearm skin area.Methods and ResultsMarstock test revealed a considerably increased cold perception threshold within the allodynic area and on the contralateral side. The patient could not perceive any warm sensation on either side. Histamine iontophoresis was not followed by any itch or pain sensations within the allodynic area or contralaterally. Nociceptive C-fiber axon reflex reactions were substantially impaired within the allodynic skin or contralaterally. Standard neurophysiological testing and quantitative vibrametry showed only mild impairment of large diameter sensory and motor fiber function at the arms. Cardiovascular reflex tests showed almost no heart rate variation indicating impairment of vagal small fiber function.Conclusions(a) Cutaneous nociceptive C-fibers do not signal dynamic mechanical allodynia. This symptom may hypothetically be due to secondary changes in the central nervous system processing that might strengthen the synaptic ties between AB-fibers and central nociceptive pathways, or due to peripheral multiplication of primary afferent low threshold mechanoreceptor input. (b) Ongoing nociceptive C-fiber input is not necessary to maintain either hypothetical mechanism. (c) Hypothetical secondary central hyperexcitability might work autonomously without any nociceptive C-fiber input for a long time or even indefinitely in some neuropathic patients.